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S2D: The Symptom to Diagnosis Podcast - Episode 29: Acid-Base Abnormalities
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S2D: The Symptom to Diagnosis Podcast - Episode 29: Acid-Base Abnormalities
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2023-06-03T00:00:00.0000000
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[upbeat intro music] [upbeat intro music] [upbeat intro music] [Dr. Cifu] I'm Adam Cifu. [Dr. Stern] And I'm Scott Stern. [Dr. Cifu] And we're here with another episode of S2D, the Symptom to Diagnosis podcast. This podcast teaches evidence-based strategies for diagnosing common medical symptoms.
We begin each episode with a case unknown to one of us. We then discuss five high yield features that help to accurately diagnose the cause of the symptom at hand. We then return to our case before finishing up with a discussion of fingerprints, common misconceptions, pet peeves, and other random pearls of knowledge. The cases that we discuss are drawn from our clinical experiences, but, because protecting patient privacy is part of our oath, we never discuss actual patients.
What are we talking about today, Scott? [Dr. Stern] We are talking about some acids and some bases. [Dr. Cifu] Aah, acid-base disorders, I like it. So you're the expert of the day. Do you have a case to present to me? [Dr. Stern] I do and we'll see if you like it when we're done. - [Dr. Stern chuckles] - [Dr. Cifu] Uh-oh. [Dr. Stern] Okay, are you ready? [Dr. Cifu] I am.
[Dr. Stern] Our patient's a 72-year-old man with long-standing type 2 diabetes since he's been about 40, who presents with mild abdominal pain, nausea, lightheadedness and shortness of breath. He really feels horrible. He says he was okay until yesterday, when he first noticed he was getting more short of breath and then felt worse and worse. He also notes that despite not eating much, his sugars are actually going up.
His past medical history is notable for well-controlled diabetes, his last hemoglobin A1C was 7.2 and hypertension. He's currently on an insulin regimen and he takes lisinopril and hydrochlorothiazide for his hypertension, which is well controlled. [Dr. Cifu] Got it. [Dr. Stern] You want his physical exam? [Dr. Cifu] Yeah, give me something. [Dr. Stern] I'm going to give you something.
So on physical exam, his vital signs - always start with those - blood pressure 102/60, his pulse is 112 and regular, his temperature is 36.5, his respiratory rate is 24 and his O2 sat on room air is 84%. - [Dr. Cifu] Huh! - [Dr. Stearn] Yeah. HEENT exam is unremarkable, his lungs show crackles a third of the way up bilaterally, cardiac exam reveals regular rate and rhythm with no murmur.
He does have a positive S4 and JVD to the angle of his jaw. His abdomen is non-tender, he has normal bowel sounds, no rebound, no guarding, and that's what I'm giving you. [Dr. Cifu] So we're doing acid-base disorders and you're not going to give me any labs. [Dr. Stern] I'm going to let you think out loud first. [Dr. Cifu chuckles] Unbelievable. [Dr. Stern chuckles] [Dr. Cifu] This might be the last podcast we do.
[Dr. Stern] Would you like some labs first? [Dr. Cifu] No, I'll do my best here. Okay. So I guess a lot of information. What jumps out to me first and foremost is clearly that this guy is hypotensive, tachycardic, tachypneic, hypoxic, right? So not in great shape. He's got rales on his lung exam. He's got JVD, he's got an S4, which is probably unimportant, I assume that probably just has to do with his long-standing hypertension, and he's a type 2 diabetic, but it looks like he's only on insulin, is that right?
- [Dr. Stern] Right. - [Dr. Cifu] Okay. And I know we're doing acid-base disorders, so I'm going to use that to frame things, it's like when you do a resident report and you're like, I know this isn't going to be a UTI, right? It's got to be something interesting. [chuckles] So I guess putting it altogether, I would say the first thing on my differential would be maybe this guy's had an MI.
It sounds like he became sort of acutely ill. He's had long-standing diabetes, so he's at pretty high risk of either, you know, a silent MI, or an atypical presentation. You can imagine after a big MI, maybe he's got some cardiogenic shock, which has led to a lactic acidosis, kind of a gap metabolic acidosis, and that's how you're going to spill over into the acid-base disorders.
I guess maybe by the same process, a pneumonia is a possibility, you know, he's not febrile, but he's an older guy, so maybe he just hasn't mounted a great fever, and again, a lactic acidosis based on that. You know, he's a diabetic and I'm going to believe that he is truly a type 2 diabetic, sounds like he was diagnosed, you know, in his 40s, so that would make the most sense, given though that he's only on insulin and I don't think you gave me insulin doses, but it's conceivable, you know, even with regular type 2 diabetes, but also if he has kind of insulinopenic type two diabetes that he could get DKA, and so we could be seeing someone who's just presenting with a little bit of DKA.
I'm not sure how I would explain the kind of fluid overload on top of that. And then I guess the other things that I'd throw out there is, you know, he's also someone with long-standing diabetes. So since we're talking about acid-base disorders, I would think about an RTA in this guy, you know, a type 4 RTA which would be common just in this population. I don't think that's like, what's getting him sick, but that might just confuse the labs.
[Dr. Stern] Sure. And so, if you were going to get labs now, what labs would you get for him? [Dr. Cifu chuckles] I'd be getting them all. I would certainly do a CBC, a CMP, I would, as soon as I get the CMP and see the low bicarb, which I'm expecting, I would want a blood gas, I'm also going to want tropes, I'm going to want an EKG. If it turns out that he's got DKA, which, again, is lower on my list, I'm going to really search for a cause of that DKA.
You know, whether it be an infection or an MI, or just, you know, non-adherence to his insulin. Now, that sounds unlikely from the sense I get from this guy, but whatever, you'll probably tell me. [Dr. Stern] And if his bicarbonate is low, are you- In addition to the blood gas, would you get any other labs? [Dr. Cifu] I'm not sure what you're asking. I guess what I'd be left with at that point is I'd say, okay, I'd want to know what the guy's anion gap is to see, is this an anion gap acidosis?
Everything I've talked about so far in the differential, which is a lactic acidosis or ketosis from diabetes would have an increased anion gap. So I think my next test would be to see, you know, what the gap is due to and see, does he have an elevated lactate level? Does he have, you know, beta-hydroxybutyrate to sort of hammer that down? [Dr. Stern] Perfect. Very well done.
[Dr. Cifu] I wasn't sure what you were going for with that. [Dr. Stern] That's what I was going for. Just to clarify, the RTA would not have an anion gap. [Dr. Cifu] Right, right. Absolutely. Absolutely. As I said, I think that would just make the interpretation of the labs even more difficult. Okay. So why don't we stop there? We've actually both talked a fair amount already and let's get to your five points of diagnosing acid-base disorders.
And I can already picture the algorithm which I've seen you write out at times, so take us through it. [Dr. Stern] All right. So the first step is, if you happen to get a blood gas, which you did, is to look at the pH because the pH is going to tell you the primary disorder. If the pH is low, the primary disorder is an acidosis. If the pH is high, the primary disorder's an alkalosis, you never compensate beyond the 7.4 range.
[Dr. Cifu] Great. That's terrific, easy place to start. It's sort of information we all learned probably in middle school, right? [Dr. Stern chuckles] Kindergarten, maybe. The next point is, once you know that it's an acidosis or an alkalosis, the question is, is it respiratory or metabolic? And that's pretty easy as well. You look at the PCO2 and the bicarbonate.
For instance, if it was an acidosis and the PCO2 is high, the primary problem's a respiratory acidosis. If on the other hand, it's an acidosis and the bicarbonate is low, the primary problem is a metabolic acidosis and so on. [Dr. Cifu] Great. Yeah, so what's the source of the acid? Is it increased acid? Is it decreased base? Is it increased base, figure it out from there? Okay. Point three.
[Dr. Stern] If it's a metabolic acidosis, which they often are, the next step is to do what you've already said, which is to get an anion gap. Because it turns out that there are metabolic acidoses that are due to acid production. And when you have acid production, the anion associated with that acid accumulates, and it's not measured and you get an anion gap. So the keto acids, the lactic acids and the uremic acids, as well as rare organic acidoses.
[Dr. Cifu] So this is the classic MUDPILES mnemonic, which you seem to not like, it's nowhere in Symptom to Diagnosis. [Dr. Stern] I don't like mnemonics. [Dr. Cifu] Huh. Well, so the only mnemonic that I remember and that I also remember what it stands for, is MUDPILES, which is the cause of anion gap acidoses. So methanol, uremia, DKA, paraldehyde, intoxication, basically alcohol, lactic acidosis, ethylene glycol ingestion, and salicylate toxicity.
I remember a lot of other mnemonics, but I can't remember what the parts of the mnemonic stand for, so I'm probably with you that I find them not terribly helpful beyond the time that you have to take the test. [Dr. Stern] I kind of resent them at an intellectual level, frankly. How do you like that? [Dr. Cifu chukles] You're such a snob. [Dr. Stern] I am. Just to finish that last thought, by the way, if people have non-gap acidosis, where the acidosis is normal, that's due to bicarbonate loss.
And so you can only lose bicarbonate from really two places, one is your bowel when you have a lot of diarrhea. And if somebody's got a non-gap acidosis from a low bicarbonate and they're not having diarrhea, then they're losing it in their kidney and that's the renal tubular acidosis. [Dr. Cifu] Right. Right, yeah, and it's just, you know, it's important to always remind yourself that we're talking about the anion gap, we're talking about the unmeasured ions, right?
And so if it's because of something that's measured, i.e. bicarbonate, you're not going to have a change in the unmeasured gap. Okay. Fourth key point? [Dr. Stern] So the fourth key point is now that you've determined what the primary disorder is, that is, an anion gap acidosis, a non-gap acidosis, a respiratory acidosis, then you have to figure out the cause, you know, if somebody has a respiratory acidosis and their PCO2 is high, well, what's going on?
Is this a neurological insult? Is this an overdose? Or is this respiratory failure from asthma, COPD, et cetera? And the same thing's true for all the other acidoses that we've already talked about. So you narrow down to which category you're in, and then you look at the differential of that category. [Dr. Cifu] And I think it's why acid-base disorders can be intimidating because a lot of the things that we've talked about, you know, whether it's diarrhea or chest pain or shortness of breath, those kind of have one differential and they may be big differentials, but it's one differential.
The fact is that when we're talking about acid-base disorders, you know, you're talking about at least four differential diagnoses, and really, once you break things down, like metabolic acidosis is gap and non-gap, you know, you're adding multiple other differential diagnoses, which you really have to know them all. [Dr. Stern] You do have to know them all. [Dr. Cifu] So let's go on to the fifth key point.
What else do you have to say? [Dr. Stern] So the fifth key point is to make sure you're not missing a secondary disorder, and one of the tricks to this is looking to see if compensation is appropriate. So whenever we have a primary acid-base disorder, the other system, i.e. metabolic or respiratory, tries to compensate to drive your pH back to normal. If it doesn't compensate appropriately, you have another problem and you have to sort that out.
So if I have a metabolic acidosis, I should hyperventilate to create a respiratory alkalosis to drive my PCO2 closer to normal. And if I'm not doing that, then I have a respiratory problem and I need to figure out what that is. [Dr. Cifu] Huh. Can I pimp you for a little bit of an example on that? [Dr. Stern] Sure. So if you have, for instance, a severe metabolic acidosis, the lowest most people are below their PCO2 down to is about 20.
There are formulas that predict these calculations that you can look up, and I wouldn't ask anyone to memorize because they're readily available. Let's say you had someone like that, and their PCO2 is near normal, like 35, that actually predicts respiratory failure in those patients. So it tells you that something else is going on and you could argue about the nomenclature. If their PCO2 is 35 and it should be 20, do you call it a respiratory acidosis, even though their PCO2 is still below normal?
I don't care about what you call it. What I care is that you recognize that it's a distinct problem that you have to address. [Dr. Cifu] Right, and I'm actually going to underline something you said that sort of lets people off the hook. You know, I spent a lot of time memorizing all of those compensation formulas, and I think that if you're not, maybe, you know, an ICU doc, who's doing this all the time, you just forget them, so it's something that I have on my phone, and you know, when I'm working on an acid-base disorder, that's when I pull it up.
And it's really, really, really, really important to use them and to do the calculations, but it's not really important to memorize them. [Dr. Stern] Totally. Do you have any other things you look for to make sure that you're not missing an additional acid-base disorder? [Dr. Cifu] This might be a little overkill since we've already talked about it, but it's just to really think about the anion gap because a significantly elevated anion gap just always suggests an anion gap metabolic acidosis.
And that's even if the bicarb is above normal, right? So even if you're dealing with a metabolic alkalosis, okay, but there's a really big anion gap, it means that buried in there as kind of a secondary disorder is metabolic acidosis. [Dr. Stern] Exactly, I agree. Great. [Dr. Cifu] Okay. So I'm going to sort of loop back a little bit because you sort of mentioned at the beginning of this, you know, if you have a blood gas, okay?
And I love blood gases, but it seems like we have blood gases less frequently than we used to. I'm not sure why that is, but the habit probably when we trained was that we were getting blood gases all the time. Now a lot of people come in maybe with venous blood gases or no blood gas at all. Are there times that you say, like, "Hey, I need a blood gas here." [Dr. Stern] Totally. So I think the reason it fell out of common use was because of the pulse oximeter.
So when you and I were in training, if you wanted to know the oxygenation, you had to get a blood gas, - Right? - [Dr. Cifu] Yeah. [Dr. Stern] And now we can get pulse oxes, but what pulse oxes don't tell you, of course, is the PCO2. So whenever you're worried about ventilation, like you got on this guy, he's breathing at 24 and you're worried about him, then you have to get a blood gas because you can have normal oxygen and still be hypoventilating.
So if I have somebody who looks like they're in respiratory distress, I'm going to get a blood gas, that is they're breathing fast, they look like they're leaning forward, they're short of breath. If I have a patient whose mental status isn't normal and they look sick, I'm also going to get a blood gas because then they might not look like they're in respiratory distress.
If I have a patient whose bicarbonate is very low, then I'm also going to get a blood gas because it's really important to see how well they're compensating or not, because that's going to affect your pH and how severely it's affected. Some other times that are less common, if you suspect carbon monoxide poisoning, you can check a carboxyhemoglobin level with the blood gas, and just in very sick patients, it behooves you to know what their pH is and what's going on in as much detail as you can.
[Dr. Cifu] Yeah, okay. Those are good rules, I think. Okay. Let's go back to the case. - [Dr. Stern] Okay. - [Dr. Cifu] Are you going to relent and maybe give me some labs with this? [Dr. Stern] I will, I will. So you asked for a comprehensive metabolic panel and a blood gas. So let me give you those. All right. So the sodium is 138, the potassium is 3.4, the chloride is 102 and the bicarbonate, are you ready?
- [Dr. Cifu] Yes. - [Dr. Stern] 10. - [Dr. Cifu] Eeh?! - [Dr. Stern] Yeah. The BUN is 67, creatinine is 1.8, I'll tell you the baseline is 1.2. [Dr. Cifu] Okay. [Dr. Stern] And the arterial blood gas pH 7.01. - [Dr. Cifu] Oh my god. - [Dr. Stern] PaCO2 of 40, Pa02 of 49, and an O2 sat of 84%. [Dr. Cifu] Wow. Okay. Interesting. So I think as I expected, right? This guy's got a metabolic acidosis as I expected, right? This guy's got a metabolic acidosis and it is a gap metabolic acidosis, you'll bail me out here, but it looks like his gap is 26?
[Dr. Stern] Correct. [Dr. Cifu] And clearly that's reflected in his blood gas and he's got a compensatory respiratory alkalosis, right? a compensatory respiratory alkalosis, right? [Dr. Stern] Wait, does he? [Dr. Cifu] No, he doesn't actually. [Dr. Stern] His PCO2 was 40. [Dr. Cifu] You're right. You're right.
So this guy's not breathing as hard as he should be, or not ventilating as hard as he should be. He's breathing pretty hard, given his tachypnea. So let me just ask you at this time, before I go on any further, chest X-ray, EKG, anything like that - at this point? - [Dr. Stern] Yeah. So chest X-ray shows cardiomegaly, bilateral fluffy infiltrates in a perihilar distribution and pulmonary revascularization, all consistent with pulmonary edema.
[Dr. Cifu] Okay, got it. [Dr. Stern] Did you say EKG? [Dr. Cifu] Yeah. [Dr. Stern] It shows sinus tach with four millimeters of ST segment elevation in V1 to V4. [Dr. Cifu] Okay. So it sounds like I'm doing pretty well right now, the only question I guess I still have is what's the cause of the acidosis and- [Dr. Stern] So before you go there though, I want to articulate for everyone what you're thinking.
So where are you now, before you even know that cause? What are you saying about his acid-base disturbance? [Dr. Cifu] Okay. So when I started with this, my differential was that this guy had had an MI, is in cardiogenic shock, and has a lactic acidosis. - [Dr. Stern] Okay. - [Dr. Cifu] Okay? My second guess, obviously educated hypothesis, really, My second guess, obviously educated hypothesis, really, was that this was pneumonia leading to sepsis and lactic acidosis, I think that's not going on now.
And my third possibility was this was DKA. As I think about this now, realizing that I'm putting As I think about this now, realizing that I'm putting my cards down on number one and/or number three, and I hope that it is one of those two, I guess what I have to worry about now is does he have both because it sounds like this guy has an MI and it might be that he had an MI and has gone into DKA because of that, and not because of cardiogenic shock.
I guess it's conceivable, I think that's probably where I'm landing right now. So I guess having talked it through that far, what I'm really interested in now, besides troponins, which I expect are going to be up and aren't going to help me a whole lot, is I'd like to know what his lactic acid is. And I guess probably beta-hydroxybutyrate as well. [Dr. Stern] And just to say, his PCO2 being 40 now tells us we have this additional respiratory problem, right?
Respiratory failure, even though his PCO2 is 40, right? So we could say he has an anion gap metabolic acidosis with a respiratory acidosis if we wanted to say it that way. [Dr. Cifu] Right. And it's interesting because I mean, his PCO2 is normal, but it should not be. [Dr. Stern] Right, should be 10, it should be- Well, people have trouble getting it down to below 20, you'd expect it to be 15 to 20. [Dr. Cifu] Yeah, absolutely. And so this guy basically has respiratory failure with a normal PCO2.
[Dr. Stern] And the reason that's important to articulate, I would just say right now is even though his PCO2 is 40, he belongs in the unit, right? So- [Dr. Cifu] So far he belongs in the unit for two reasons. Let's see how many others he's got. [Dr. Stern] So his lactate is 1, normal is less than 1.2 in our lab and his beta-hydroxybutyrate is 14, normal is less than 0.5. [Dr. Cifu] Wow. Have I heard a glucose?
- [Dr. Stern] Yes, at 543- - [Dr. Cifu] Okay. [Dr. Stern] -and his troponins are 874, high sensitivity, normal is less than 22. [Dr. Cifu] Wow, this guy is sick. So what we have now is that this is a guy with an acute ST elevation MI and DKA, this is a guy with an acute ST elevation MI and DKA, both of which need to be treated urgently basically. And so, you know, we need to intervene quickly on his DKA while we're getting him buffed up for the cath lab.
[Dr. Stern] Yeah. This is a guy who should frighten you a lot. [Dr. Cifu] Yes. Okay. [Dr. Stern] Well you did well, you did well. You know, wipe the perspiration from the brow. [Dr. Cifu] Yeah, I was going to say, let me fan myself off, and then we'll move on to our famous fingerprints, and then we'll move on to our famous fingerprints, common misconceptions, pet peeves, and random pearls of knowledge.
That was actually a stalling factor because I forgot what the four things were because I was so stressed out by the case. You got any fingerprints? [Dr. Stern chuckles] No. Do you? [Dr. Cifu] I have a terrible fingerprint. And I'm only saying this because as I was reading through Symptoms to Diagnosis preparing for this, I found this fingerprint and I was like, we got to get this fingerprint out of the book, this is terrible.
So it comes when discussing respiratory acidoses So it comes when discussing respiratory acidoses and discussing signs for respiratory failure, and it turns out that a pulsus paradoxus of over 25 has a likelihood ratio of 23 for severe asthma. I don't even know what severe asthma is, but sure. A really high pulsus paradoxus in someone who's breathing really hard is a bad thing. [Dr. Stern chuckles] Okay. Well, thank you for that.
[Dr. Cifu] Common misconceptions. [Dr. Stern] I think the one I want to highlight that the case highlights is that people often feel that DKA only occurs in type 1. As most of us know who've been in practice for a long time, type 2 diabetes is at least 50, if not 100 times more common than type 1, and so although DKA is less common in type 2, because there are so many more patients with type 2 diabetes, and type 2 diabetes actually accounts for a lot of DKA.
If you look at all the cases of DKA, 12 to 47% of patients who present with DKA actually have type 2 diabetes. You'd alluded earlier that maybe with a long-standing diabetes, even type 2, that patients are more likely to get insulinopenic, and that's probably part of the pathophysiology that we have more beta cell failure in long-standing type 2s, but for whatever the cause, type 2 diabetes can and absolutely does lead the DKA.
[Dr. Cifu] That's a great point. And it's probably worth underlining that in a patient with DKA- Or well, type 1s are more likely to go into DKA, but there are just so many type 2s out there. And I got to say, I mean, most of the people who you admit with, like DKA as the primary problem are type 1, right? Most of the type 2s who I feel like I take care of on the inpatient service who have DKA are sort of coming in with something else, have a little DKA on the side, right?
And it's certainly there, it certainly needs to be paid attention to, but I don't think of it as, you know, like, oh, pH of 7 needs to be in the unit immediately. [Dr. Stern] I think the reason we think about it differently is type 1 patients are much more predisposed to DKA, even if they omit their insulin. And probably type 2 patients often need an additional stressor in the counterregulatory hormones to push them far enough to go into DKA, and then that dominates often the course of the illness.
[Dr. Cifu] Yeah, great point. I have a common misconception. [Dr. Stern] Go ahead. [Dr. Cifu] This is sort of a classic, but I think the misconception is that DKA is associated with increased body potassium, right? People almost always present with hyperkalemia and most people know that you don't need to treat that hyperkalemia because as you treat the diabetes, right? As you give people insulin, as you make them less acidotic their potassium is going to come down.
But the fact is that most people's total body potassium is low and that's because K is lost with the osmotic diuresis that they have with glycosuria, and also because a lot of the times these people are hypovolemic, and so they have hypovolemia-induced hyper aldosterone states, which leads to more potassium loss. Generally what's going to happen is these people come in with really high serum potassium, which comes down to normal very quickly as you treat their DKA and then generally need to have their potassium repleted as you get them sort of really beyond the DKA, back to normal.
[Dr. Stern] That's a good point. I mean, we don't spend a lot of time in this podcast talking about treatment, but actually if a patient comes in with DKA whose serum potassium is already low, like in the 3.3 area, the recommendations are to treat their potassium before you give them insulin. [Dr. Cifu] Right, you know, I find that actually is an important point in like an urgent care setting where very often we'll have people come into urgent care, they'll get a finger stick, their finger stick will be 500, right? And the first thing to do is to say, wow, you know, give this person 10 units of insulin.
And I usually feel like, you know, maybe the first thing to do is a stat BNP because let's see what their electrolytes are, because look, you know, their sugars probably been that high for the last 12 hours, and if we wait another 20 minutes, it's not going to be a big deal. While if I give them, you know, 10 of insulin and their K is 2.5, I could kill them. [Dr. Stern] I think that's totally right.
[Dr. Cifu] What are we up to? - [Dr. Stern] Pet peeves. - [Dr. Cifu] Pet peeves. [Dr. Stern] All right, so my pet peeve has to do with the pulse ox. So, you and I were trained before those were available, and now it seems to me that everybody thinks if your pulse ox is okay, that your blood gas would be okay. And the reality is, if you do an AA, you know, alveolar air equation and you calculate somebody's labs, you can actually prove that people can have totally normal oxygen saturations, especially on supplemental oxygen, despite the fact that they're markedly hypoventilating.
So I said that backwards a little bit, but nonetheless, you have to check a gas if you're worried about ventilation because the PaO2 and the SaO2 can be fine. [Dr. Cifu] I thought you were going to, like, try to convince me that pulse oxes are unnecessary, but fortunately you didn't go in that direction. [Dr. Stern] No, that might've been 15 years ago, I might've said that, but not now. Okay, I finally bought into that. All right, do you have one?
[Dr. Cifu] So my pet peeve is the venous blood gas. I don't like venous blood gases. I feel like they're sort of an excuse that we didn't get an ABG, but we have a VBG, so that's okay. The fact is venous blood gases are really quite good for pH, right? We usually say the pH in a venous blood gas is, I don't know, like 300ths of a point off from the arterial blood gas, which is kind of unimportant, but venous blood gases are not so good for measuring PCO2, and I think as you just said, the reason to get an ABG is to measure PCO2, so if you want to know the PCO2, you got to get an ABG.
[Dr. Stern] I agree, that bugs me. The data says it's not accurate. [Dr. Cifu] Huh, we agree on a pet peeve. [Dr. Stern] How do you like that? [Dr. Cifu] Clinical pearls. [Dr. Stern] Okay. So I don't know if you'll agree with this or not, but I suspect not, but we do have to have a low threshold for checking serum lactates, they weren't really available- [Dr. Cifu chuckles] Oh, Jesus Christ.
[Dr. Stern] Listen, just because they weren't available when we were trained, doesn't mean they're not useful. Listen to this statistic. If you look at infected patients who are normotensive, the mortality if the lactate was over 4 is 15% versus it's under 2.5% if their lactate levels are less than 4. There's good prognostic information in normotensive septic patients. [Dr. Cifu] Can I tell you how little I care about that little piece of data that you threw at me?
[Dr. Stern stammering] That's a big mortality difference! [Dr. Cifu] I know but that's assuming that a physician caring for the person has no idea that this person is sick, right? And I think the fact is that most of the time, when like, you know, you get called that oh my God, this person's lactate's up, what you do is you sit back and just say, "No kidding." You know? "The person's sick!" [Dr. Stern] Well, let me point out that not everyone has your experience, A.
So it's true and it's not trivial, right? We have lots of people who are seeing patients who are a year or two in practice. Second of all, you know that we have colleagues who study doing various reviews of lab results and have been able to predict carts 48 hours before physicians. So I think that you are minimizing useful data. [Dr. Cifu] Well, I think though that we are lacking outcomes that actually- Being able to predict that makes a difference, I think what we know is that we send people to the unit faster, but we don't save lives with it.
[Dr. Stern] Okay, well, if I'm in the hospital, I'm just going to ask you, since you're my physician, please check a lactate level, I'd rather not have the cart before I end up in the ICU, I'd rather end up in the ICU before the cart. [Dr. Cifu] Sounds fine. [Dr. Stern] Can we agree with that? [Dr. Cifu] I will put an A line in and measure it Q hour- Actually, I'm not going to put it an A line in, I'm going to stick you every hour for the lactate.
[Dr. Stern] Oh my God. You're so mean to me. Okay. Do you have one? [chuckles] [Dr. Cifu] I do. So this is again, not a brilliant insight, I feel like I'm lowering expectations of everything I say today. Most of the unmeasured anion of everything I say today. Most of the unmeasured anion in the anion gap is albumin, right? Thus, if the albumin is low, the normal anion gap will be less than the usual, what I remember is 12, it's really 8 to 16 and it varies lab to lab, and it falls in a predictable way.
So the anion gap falls by 2.5 mEq/L for every 1 g/dL drop in albumin. And it's important because, you know, we're mostly thinking about this in the hospital, many people we take care of in the hospital have albumins of 3 and even 2, and that makes a really big difference in the anion gap. [Dr. Stern] The other thing is to know your own hospital's normal anion gap.
It turns out to vary quite a bit from hospital to hospital. [Dr. Cifu] Right. I think some anion gaps actually include the potassium in the anion gap while others don't. [Dr. Stern] Well, and the normal range because apparently they use different machines. [Dr. Cifu] Oh, okay, I didn't know that. [Dr. Stern] All right. So my next pearl was, well, we've already mentioned this, so I'll just say it briefly, is poor respiratory compensation predicts respiratory failure.
[Dr. Cifu] Right, makes sense. Mine, I also sort of mentioned before when I talked about the, I don't know, the subsequent differential diagnoses, is that you got to find a cause of DKA, right? So if someone comes in with a diabetic ketoacidosis, that's most likely a symptom, right? Well, let's just say that is a symptom and not the cause. And the cause might be, I haven't taken my insulin in three days, but it might also be, you know, I've got an infection which isn't clear, I've got an MI, I've got pneumonia, you know, something which has caused the person to go into DKA.
[Dr. Stern] As a matter of fact, studies showed that's the most common cause of death in DKA, it's the underlying cause of the DKA. So if you don't identify that, you're making a big mistake. So I really agree with that. [Dr. Cifu] There was an interesting piece of data in Symptom to Diagnosis that I actually tweeted about last week that looked at the cause of abdominal pain in type 1 diabetics with DKA because abdominal pain is very, very, very common with DKA.
Sometimes it's abdominal pain just from the ketoacidosis, and sometimes it's abdominal pain from an abdominal process that's causing the ketoacidosis. It turns out that people with the most severe acidosis, it's mostly due to the DKA and people with less severe acidosis, it's actually most commonly due to what's causing it. [Dr. Stern] Right, totally. And I think you have the last- No, we have two more pearls.
[Dr. Cifu] Okay. [Dr. Stern] So mine is, it's important if somebody has respiratory failure and a respiratory acidosis to determine whether it's a chronic or an acute respiratory acidosis. So, you know, oftentimes it's clinically apparent, someone comes in with long-standing COPD, and they're not really feeling that much different than normal and you get a blood gas and their PCO2 is 50 and their bicarbonate is high, you're not that worried.
And other patients have an asthma attack and they just got sick, and so it's obvious it's acute, but if you're not sure, the labs can help you. So in acute respiratory failure and in acute respiratory acidosis, the kidney doesn't have much time to reclaim bicarbonate. So that in an acute process, the bicarbonate only goes up by about 1 mEq for every 10 mm that the PCO2 goes up. about 1 mEq for every 10 mm that the PCO2 goes up.
On the other hand, in chronic respiratory acidosis, the kidneys have more time and the bicarbonate goes up by about 3 mEq for every 10 mm that the PCO2 goes up. So looking at the bicarbonate, even if you don't have an old blood gas or you don't have a good clinical context of whether this is acute or chronic, can give you a sense of whether it's acute or chronic. And let's face it, that makes a difference because if it's chronic, it's much more likely to be somewhat quasi-stable, and if it's acute, it's not.
[Dr. Cifu] Yeah. I would just underline that and say that, those people who are coming in with, I don't know, pending respiratory failure, those are absolutely the people to get the blood gas, pull out your calculator, do the calculations and say, is this where the person lives, right? Because we see a lot of people, right, who live with a PCO2 of 50 or 60, but you want to know if this is acute or chronic.
[Dr. Stern] Right. [Dr. Cifu] And I'm right to say that compensation for metabolic disorders happen faster than compensations for respiratory disorders. [Dr. Stern] Right, so when you have a metabolic disorder, you can hyperventilate immediately. So there's not two formulas for compensation for metabolic acidosis, there's only one and the same for metabolic alkalosis, but for the respiratory problems where your kidney has to compensate, then there's both acute and chronic compensation because the kidney takes more time.
[Dr. Cifu] So my very last point, since we're running on a little bit long, and this may be flogging the proverbial lactic acid horse, or whatever, how many metaphors am I mixing there? So this is just to help you to remember, you know, what causes lactic acidosis, because jeez, like anything causes lactic acidosis. So lactic acidosis is caused by anything that impairs oxygen from getting from the environment, right, the outside world to the mitochondria, to go to the smallest level possible.
So the differential can be remembered by tracing oxygen from the outside to the cells. Hypoxia can cause lactic acidosis, carbon monoxide, which prevents hemoglobin from carrying oxygen, cardiogenic, septic, hypovolemic shock. And then, even like focal vascular obstruction, right? So you've clotted off a leg, right? So you're not getting oxygen into one part of your body. And then maybe at the lowest level cyanide poisoning, right?
Which blocks electron transport in the mitochondria is probably as far down as you can get. Can you get further down than me there? [Dr. Stern] That's all I got. [Dr. Cifu] Okay, good, good, because we're out of time. So we hope you found this episode of S2D, the Symptom to Diagnosis podcast useful, and a bit enjoyable. As a reminder, our textbook, Symptom to Diagnosis An Evidence-Based Guide takes a much deeper dive in how to think about and reason through the diagnosis of medical presentations.
The book is available in print through all the usual places, on your mobile device and also available and fully searchable via the AccessMedicine website available worldwide from McGraw Hill. The music for the S2D podcast is courtesy of Dr. Maylyn Martinez. [upbeat outro music] [upbeat outro music] [upbeat outro music]