The Order and Disorder With Acid-Base Basics
In this episode, Dr Harrison speaks with Paul Shiu, DO, about the order and disorder of acid-base basics, including the interpretation of arterial blood gases (ABGs) and the various respiratory and metabolic disorders that cause abnormality in ABGs.
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Anil Harrison, MD, is the associate program director of the internal medicine residency program and the ambulatory care director at Touro University and St Joseph’s Medical Center-Dignity Health (Stockton, CA). Dr Harrison is board certified in India and the United States.
Paul Shiu, DO, is a second-year internal medicine resident at St Joseph's Medical Center (Stockton, CA).
Dharminder Singh, MD, is an internal medicine chief resident at St Joseph’s Medical Center (Stockton, CA).
Jessica Bard: Hello everyone. And welcome to Multidisciplinary Dialogue, Clinical Rounds and Case Reviews with your host, Dr Anil Harrison, Associate Program Director for the Internal Medicine Residency Program and the Ambulatory Care Director at Toro University and St. Joseph's Medical Center, Dignity Health in Stockton, California.
Today, we have a grand rounds episode for you with Dr Paul Shiu, who is a second-year internal medicine resident at St. Joseph's Medical Center in Stockton, California. On this episode, we'll discuss arterial blood gases, the order and disorder with acid-based basics. The views of the speakers are their own and do not reflect the views of their respective institutions.
Dr Paul Shiu: So, Dr Harrison, for our first podcast, what do you want talk about? What should we talk about?
Dr Anil Harrison: Well, Paul, I was approached by some residents on doing podcasts and the request was to start with arterial blood gases and we have a fair number of podcasts on the evaluation of ABGs, though we will start off with the very basics and subsequently follow it up with various respiratory and metabolic disorders, causing an abnormality and how to evaluate them.
Dr Paul Shiu: I was on ICU not too long ago. And I remember everyone said how important it was, how fundamental it was, to be able to interpret arterial blood gases, the title of our podcast, our first podcast is The Order and Disorder With Acid-Base Basics. Dr Harrison, why do we do arterial blood gases?
Dr Anil Harrison: That's a great question, Paul. Arterial blood gases can be considered as an indirect measure of what might be going on in the human body. The problem could be at the cellular level or the respiratory system or with the kidneys or the gut, the nervous system, or it could be a combination of some or all of them.
Dr Paul Shiu: I know that our listeners are very smart and they're very motivated. They want to learn as much as possible, regardless of what stage in training they are, whether they are a student, an intern, a resident, and hopefully, if you guys are out there, attendings too. So we want to keep this nice and informal. This is a conversation between Dr Harrison and I. And we want to share this conversation with the world, hopefully, that will prove beneficial. I have a tendency to ramble, but Dr Harrison also is a funny guy. Dr Harrison, just off the cuff, not that this is scripted or anything. Do you have any jokes for us?
Dr Anil Harrison: Well. I'll tell you one. Just a couple of days ago, I was talking to a gastroenterologist colleague of mine and was telling him about us doing the blood gases and asked him if he would be interested. And his reply was "Anil, I have enough of other kinds of gases to deal with. Thank you. But no, thank you."
Dr Paul Shiu: Which is a perfect opener to ABGs. Dr Harrison, please, I implore you, before we go into ABG cases, can we just talk a little bit about the basics first?
Dr Anil Harrison: Absolutely. Paul. So let me start off by saying the arterial pH and pCO2, which stands for the partial pressure of carbon dioxide, they work very closely. The closeness is demonstrated by if you take a mobile pH of 7.40 noticeably the numbers after the decimal are 40, which by the way, is a normal pCO2. The bond between the arterial pH and PCO2 is such, they're very determined to keep our bodies in balance. So, I'll give you an example. If the pH changes from 7.40 to 7.50, which is an increase by 10 behind the decimal, the pC02 moves in the opposite direction by 10 points and changes from 40 to 30.
Conversely, if the pH falls from 7.40 to 7.30, the pC02 goes up by 10 from 40 to 50. The relationship between pC02 and the serum bicarb, the latter depends of course on the kidneys, might seem distant. However, they agree on keeping the distance at 15, under most conditions. So with a normal bicarb of 25, the pC02 ought to be, 25 plus 15 equals 40. As an example, if the serum bicarb drops from 25 to 20, the pC02 should change to 20 plus 15, which equals 35. Signifying a drop of five in the pC02 as well.
What this means in simple terms Paul, is something has happened in the body, which has resulted in a mild metabolic acidosis. The lungs, therefore, have to compensate appropriately by blowing off carbon dioxide to keep the pH of the blood close to normal.
Conversely, if your serum bicarb increases to 30 from 25, this signals the brain to slow down the respiratory drive, resulting in the retention of pC02, causing it to change from 40 to about 45, in trying to maintain the pH within normal limits.
Dr Paul Shiu: Huh. So it would make sense that if the pC02, the cause of pressure of carbon dioxide goes up, denoting an excess of pC02, the pH would then move in the opposite direction.
Dr Anil Harrison: Correct.
Dr Paul Shiu: Which I guess we refer to as respiratory acidosis.
Dr Anil Harrison: Absolutely true. Yes.
Dr Paul Shiu: And then conversely, if the pC02 moves downwards that signifies that the lung is blowing off excess carbon dioxide and the pH then moves in the opposite direction, signifying a respiratory alkalosis.
Dr Anil Harrison: You got it, Paul.
Dr Paul Shiu: Ah.
Dr Anil Harrison: That is true.
Dr Paul Shiu: Dr Harrison, what if the pC02 and a pH moved in the same direction though?
Dr Anil Harrison: Well, this signifies that the bicarbonate is misbehaving.
Dr Paul Shiu: Oh, how mischievous.
Dr Anil Harrison: And therefore points towards a metabolic problem. An example would be if the pH drops from let's say 7.40 to 7.30, and the pC02 also drops, this suggests a metabolic problem, metabolic acidosis. And when the pH increases from 7.40 to 7.50, the pC02 is also up or is increased. This suggests a metabolic alkalosis.
Dr Paul Shiu: Amazing, absolutely amazing. And for those tuning in, I just want to throw in one little nugget or pearl that Dr Harrison is trying to explain. Let's introduce some normal values. The normal pH of blood is from 7.35 to 7.45. And therefore, based on what Dr Harrison has explained, the normal pC02 is therefore between 35 and 45, the last two digits of the pH. If a pH less 7.35 confirms acidosis, while a pH greater than 7.45 confirms alkalosis and normal serum bicarb ranges from 22 to 28.
Dr Anil Harrison: Well, I would like to point out that with blood gases +-3 is considered within the range, a normal pO2, by the way, is between 80 to 100.
Dr Paul Shiu: Normal arterial blood gases reads in a very particular format. Normally when it's listed, the numbers all occupy a specific slot. So for instance, if I read off the following numbers, 7.40, 40, 80, 25. This order is understood to mean pH, pCO2, pO2, and serum bicarb, 803.
Dr Anil Harrison: Absolutely. Paul. So let us talk a little bit about the individual respiratory and metabolic components. Carbon dioxide is produced with cellular respiration and pCO2, which is the partial pressure of carbon dioxide, represents the respiratory component. The pCO2 can change rapidly in minutes to try and compensate in an attempt to normalize one's pH. It would make sense with the problem occurring within the body and the respiratory drive is suppressed, active breathing slows down and results in an increase in the pCO2.
Dr Anil Harrison: Conversely, if the respiratory drive increases the lungs blow off more of carbon dioxide resulting in a low pCO2. So this actually makes perfect sense that the respiratory drive can either be normal, slow, or fast. Therefore, with issues, within our bodies, one can either have a respiratory acidosis or a respiratory alkalosis, but never both simultaneously.
Dr Paul Shiu: Well, wait Dr Harrison. Let me just ponder that thought for a moment. So you're saying that respiratory acidosis and respiratory alkalosis cannot happen-
Dr Anil Harrison: Together? No, it can't, correct.
Dr Paul Shiu: ... simultaneously. Right, together. So it's a fun exercise to imagine, we have two pairs of lungs, but one wind pipe. So if you're breathing really fast, you can become alkalotic because you're ridding your body of CO2. If you're breathing slow or having shallow breathing, then you're going to retain CO2 and that makes you acidotic.
Dr Anil Harrison: Absolutely, Paul.
Dr Paul Shiu: Ah, it makes sense now, Dr Harrison.
Dr Anil Harrison: Good. The bicarb regulation that occurs in the kidneys, though the kidneys take days to compensate. Now, this is in contrast to the respiratory issues where the lungs take just a few minutes to compensate. Interestingly enough, because serum bicarb is controlled by more than one organ, the kidneys, the gut, and the transcellular shifts. Therefore, one can have more than a single metabolic abnormality at the same time.
Dr Anil Harrison: One can have a HAGMA, a high anion gap metabolic acidosis, along with NAGMA, normal anion gap metabolic acidosis. Or you could have a HAGMA and a metabolic alkalosis or NAGMA, along with a metabolic alkalosis.
Dr Paul Shiu: HAGMA, If I recall correctly, Dr Harrison, stands for high and gap metabolic acidosis. And NAGMA stands for normal and gap metabolic acidosis. Is that correct?
Dr Anil Harrison: Correct. Paul.
Dr Paul Shiu: Excellent. So now that we have laid out the groundwork, can you give us a cue on the sequence of how to approach ABGs?
Dr Anil Harrison: Absolutely, Paul. So let's start off with some simple examples., a pH of 7.20, a PCO2 of 30, a pO2 of 80 and a serum bicarb of 15. You'd agree, Paul, that the pH is below 7.35, so this is acidosis. The next thing is to look at the pCO2, which as we discussed, has to move in the opposite direction. So if the pCO2 is below normal, or let's say a pCO2 of 30 in this case, which instead of moving in the opposite direction has moved in the same direction as the pH, this suggests that this is a metabolic problem. And then you look at the bicarb, the bicarb is 15. So you would say that this person has primarily a metabolic acidosis.
Dr Anil Harrison: Now, if you add 15 to the current bicarb, of which is also 15, this would give one the expected pCO2. And as you know, 15 plus 15 is 30. And if you look at the patient's pCO2, which is also 30. Therefore, you would describe this as primarily a metabolic acidosis, with a normal compensation by the lungs.
Now let's take another example where let's say the pH is 7.50, pCO2 of 50, pO2 of 80 and a bicarb of 35. A pH of 7.50 is alkalemia. Now notice the pCO2 has moved in the same direction as the pH and is 50. This points towards a metabolic issue. Then you look at the bicarb, it's 35. This confirms it to be a metabolic alkalosis. The next thing you do is you add 15 to the serum bicarb of 35, and that should give you one's expected pCO2, which is 50.
And the pCO2 of the patient is also 50. So, therefore, you could say that this person primarily has a metabolic alkalosis with adequate compensation by the lungs.
Another example would be a pH of 7.30, a pCO2 of 50, a pO2 of 80 and a bicarb of 35. A pH 7.30 confirms acidosis. And with a pCO2 of 50 confirms a primary respiratory problem because they're moving in the opposite direction. And so therefore you could call this primarily a respiratory acidosis. Noticeably the kidneys have compensated well with a bicarb of 35. And by the way, if you 15 to the bicarb of 35, it equals a pCO2 of 50, as in this case.
Dr Paul Shiu: Remarkable.
Dr Anil Harrison: I'll give you another example, Paul. A pH of 7.50, a pCO2 of 30, a pO2 of 80 and a bicarb of 15. A pH of 7.50 confirms alkalosis and since the pCO2 is in the opposite direction of the pH, it confirms it to be primarily a respiratory problem, a respiratory alkalosis. And by the way, the kidneys have responded well by dumping alkaline carbonate or retaining hydrogen ions, hence the bi-carb is low. And if you add 15 to the current bicarb, which is also 15, it equals 30. Which is the expected and confirmed pCO2, confirming this to be primarily a respiratory alkalosis.
Dr Paul Shiu: Dr Harrison, this is extremely hero. We have covered every possible permutation. So, we've covered an example of metabolic acidosis, an example of metabolic alkalosis, an example of respiratory acidosis and the example or respiratory alkalosis. So my question right now is, because I remember medical school we learned that there were other ways of determining or rather... No, it is determining the expected pCO2, I believe that's called Winters Formula.
Can you explain all the various ways of linking the relationship between pCO2 and bicarb?
Dr Anil Harrison: Absolutely. Paul. So if you're working in the ICU or the CCU, the easiest one is to add 15 to a person's bicarb and that should be corresponding to the person's pCO2. So remember the number 15. If you want, you can use the Winter's Formula, which is the pCO2 equals 1.5 times the serum bicarb, plus eight, plus minus two. And you will realize this calculation is pretty close to the one that we just discussed of adding 15 to the serum bicarb.
If you have to be really diligent, there is a third way of doing it. And that is by using the Winter's Nomogram, which details subtle changes depending on if the problem is acute or chronic, with either a metabolic or a respiratory problem.
So if you look at the Winter's Nomogram along the X-axis, we have the arterial pH and along the Y-axis, you have its best friend, the pCO2. Increased pCO2 of 40 signifies hypoventilation, while a reduced pCO2, which is below 40 signifies hyperventilation, so you're blowing off carbon dioxide. With a Nomogram one concentrates on the bicarb to the pCO2 ratio. With acute respiratory acidosis the ratio of bicarb to pCO2 is about one is to 10. Which means with acute respiratory acidosis, as the pCO2 goes up by 10, the bicarb moves up by one point. Whereas, with chronic respiratory acidosis, where the kidneys have had some time to compensate, the ratio becomes one is to three. Which means for every three-millimeter increase in your pCO2, the bicarb has had time to increase by one milligrams per liter.
In contrast, with the respiratory alkalosis, if it's acute, the ratio of bicarb to pCO2 is one is to five. Whereas, with chronic respiratory alkalosis, the ratio is one is to two. Now, if it's a metabolic issue such as metabolic acidosis, the ratio of bicarb to pCO2 is once to one, whereas with metabolic alkalosis, the ratio of bicarb to pCO2 is two is to one.
Dr Paul Shiu: Dr Harrison. This third method, I'm just pondering. Very involved because it requires some values to keep in the back of one's mind. The rule of 15 really is quite convenient, especially in a fast-paced environment at the ICU.
Dr Anil Harrison: Absolutely. It's very easy to do.
Dr Paul Shiu: Now that we've covered and laid out even more of a foundation of ABGs, could you explain for us the pathophysiology in just simple terms, please give us some examples of metabolic acidosis and alkalosis as they relate to the kidneys.
Dr Anil Harrison: Sure, Paul. As we know carbon dioxide plus water equals bicarb plus hydrogen ions. So a person, for example, who's vomiting, who has emesis is losing hydrogen ions, which can result in a metabolic alkalosis. So the serum bicarb will be elevated and to compensate, the lungs will slow down and therefore the pCO2 might be elevated. Conversely, if a person has severe diarrhea, there is loss of bicarbonate, and therefore this can result in a metabolic acidosis, with the serum bicarb being low. And the lungs will compensate by blowing off more CO2 causing the pCO2 to be low.
Dr Anil Harrison: Within the kidneys, Paul, there can be a loss of bicarbonate causing a metabolic acidosis, which happens either because of a reduction in the absorption, in the proximal tubules. For example, with Fanconi syndrome or with conditions causing a proximal RTA or a type 2 RTA, or there can be an issue getting rid of hydrogen ions or acid in the urine, which is what happens with Type 1 or distal RTA, resulting in a metabolic acidosis, your distal Type 1, renal tubular acidosis.
Dr Paul Shiu: This is all bringing back a very pleasant memory from basic sciences in medical school. I'm sure every one of you, with tuning in, attests to this funny feeling that I feel right now. But isn't there a Type 4 renal tubular acidosis and what happens over there?
Dr Anil Harrison: Sure. Paul, so with Type 4 renal tubular acidosis, which can also result in a metabolic acidosis and it’s usually a normal, in nine gap metabolic acidosis. There is a lack of the Renin-angiotensin-aldosterone-axis. And so therefore this results in a deficiency in aldosterone and therefore sodium and bicarbonate are not reabsorbed efficiently, causing a low sodium along with metabolic acidosis. On the flip side, as with Cushing disease, the excess aldosterone acting on the distal convoluted tubules results in excessive sodium, being reabsorbed along with bicarb, resulting in a metabolic alkalosis with an elevated blood pressure.
Dr Paul Shiu: We covered so much ground.
Dr Anil Harrison: We did.
Dr Paul Shiu: In surprisingly, a short amount of time. So I think what is the modern parlance now in medical school, high yield? I think this is high yield Dr Harrison, don't you agree?
Dr Anil Harrison: I hope so.
Dr Paul Shiu: Well, we'll let the audience decide. We'll let them vote with their peers. We hope that you will tune in with us next time as well, before we conclude this first podcast, tell us one more joke, please.
Dr Anil Harrison: Paul. Okay. A man is rushed to the hospital and is given blood. And when the man gets worse, a nurse goes running to the doctor saying, "We gave him the wrong blood." The doctor responds, "Ah, must have been a typo."
Dr Paul Shiu: Ah. Type O. Thank you so much, once again, everyone for tuning in on our first Dr Harrison's podcast with this trusty sidekick, Paul.
Dr Anil Harrison: Thank you, Paul. That is tremendous.
Dr Paul Shiu: Thank you, Dr Harrison. Thank you all.