Time Stamps

  • 01:45 Pearl 1: Evidence for potassium repletion 
  • 09:10 Pearl 2: Framework for hypokalemia
  • 17:09 Pearl 3: Repletion goals
  • 23:00 Pearl 4: Options for hypokalemia treatment
  • 29:13 Pearl 5: Frequency of lab checks and repletion

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Show Notes

Pearl 1:  How much of a deficit is hypokalemia and what is the evidence behind repletion?

  • Hypokalemia 
    • Defined as K < 3.5 mEq/L
      • Can be from total body deficit or intracellular K shifts 
      • Variation on exact amount deficit:  
        • Some quote 1 mEq below 4 = 100-200 mEq deficit vs. every 0.3mmol is 100 mEq of K+ deficit
        • Note: Does not account for ongoing K losses

Pearl 2:  Causes of Hypokalemia

  • Four MAIN buckets!
    • Poor oral intake:
      • Less common
      • <1 g intake/day
    • Excretion in the urine:
      • Increased distal delivery of Na + Cl
      • Type 1 & Type 2 Renal Tubular Acidosis (RTA)
        • Think for hypokalemia + non-anion gap acidosis
      • Excretion with non-absorbable anions. Example:
        • Excess [bicarbonate] with vomiting or NG suction
          • Excess [bicarb] will be urinated out and takes K+ along with it!
        • Antibiotics: IV Penicillin in large doses, aminoglycoside
        • B-hydroxybutyrate in DKA
      • Osmotic diuresis Ex:
        • Hyperglycemia
        • Urea excretion after relief of chronic urinary obstruction
      • Hypomagnesemia –> K+ wasting
      • Mineralocorticoid excess
    • GI loss:
      • ABOVE: Vomiting/NG Tube losses
        • Loss of Cl rich fluid → Increased [bicarbonate] → excess bicarb will be urinated and takes K+ along with it 
        • So technically a urinary loss
      • BELOW: Diarrhea/Laxatives/Enemas
        • Anything that increase stool volume can lead to K loss through the GI tract
    • Intracellular shifts:
      • ↑ B-adrenergic activity (Catecholamines)
        • Increased epinephrine → K into cells
          • Activate Na/K pumps
        • Examples of highly adrenergic states:
          • Acute MI
          • Alcohol withdrawal
          • Panic attacks (anxiety & hyperventilation)
      • Insulin
        • “Insulin also pushes potassium in to cells”
        • Promotes Na/K-ATPase activity and pulls K+ into cells
      • Alkalemia
        • Favors K+ into cells and H+ out of cells
      • ↑ Hematopoietic cell production
        • ↑ K+ uptake by new cells
        • Ex. GM-CSF, vitamin B, folic acid
      • Rare: periodic paralysis, hypothermia

Pearl 3:  What is the goal for K+ repletion?

  • Normal range:  3.5 – 4 mEq/L
    • Goal is WITHIN this range
      • Depending on the patient:
        • Examples:
          • Patient on diuretic
            • Continuous loss of K → more aggressive repletion
        • Patient with uncomplicated pneumonia
          • Low risk for ventricular arrhythmia → less aggressive repletion
    • Urgency of K repletion is patient dependent
      • More urgent (patients who may have a more sensitive myocardium)
      • Less urgent (avoid repleting to 4.0 exactly)
        • No cardiac risk factors
        • Good PO intake
  • What about long-term, chronic low K? 
    • May cause metabolism issues and linked to other adverse outcomes
      • High K diet →  Decreased incidence of stroke, cardiovascular events, and mortality

Pearl 4:  How to replete potassium?

  • IV vs. PO
    • If they have a gut, try to use it!
      • If the patient has GI distress, divide into multiple doses over the course of the day
    • IV can be limited in that small mEq are given an hour infusion.
  • Multiple K+ supplements are available
    • Consider what ELSE the patient might need
    • Potassium chloride
      • If patient has metabolic alkalosis
    • Potassium phosphate
      • If patient  has phosphate deficit
    • Potassium citrate (especially for outpatients!)
      • If patient has kidney stones
        • Citrate is a natural stone inhibitor that chelates calcium
      • If patient has hypocitraturia 
    • Note: Potassium phosphate & citrate are also on K rich foods like figs, dried fruits, and avocados! 
  • What are other options?
    • Check the patient’s medications! 
    • Is there something causing kaliuresis? (urinary potassium excretion)
      • Furosemide
      • PPIs
        • Can lead to hypomagnesemia which can lead to hypokalemia
      • Fluids

Pearl 5:  When to order potassium labs?

  • Do we over check labs? 
    • Often we check twice a day for patients who are undergoing diuresis
      • Decide based on the clinical scenario:
        • Ex: patient is not urinating much (low diuresis)
          • Don’t need to check labs! 
    • Think if routine morning labs are needed for you patient
      • Harms of checking labs that are not needed
        • Time (of everyone involved)
        • Patient comfort
        • Money
  • Changing practices around labs and repletion
    • Requires interdisciplinary education
    • Requires a range of physicians (interns to attendings) to change the framework of when to replete K!

Transcript

Dr. Shreya Trivedi: Welcome to the Core IM 5 Pearls Podcast, bringing you high-yield evidenced-based pearls. I’m Dr. Shreya Trivedi

Dr. Ben Osher: I’m Dr. Ben Osher, an internal medicine resident at BIDMC. On today’s 5 Pearls episode, we’ll be talking our practices around repletion. Today we’ll be covering potassium, and next episode will be mag, phos, and the bigger picture on electrolytes!

Dr. Shreya Trivedi: Yep! Let’s get started with the pearls we’ll be covering in this episode. Test yourself by pausing after each of the 5 questions. Remember the more you test yourself, the deeper your learning gains.

Dr. Ben Osher: Pearl 1 – Evidence for potassium repletion. 

Dr. Shreya Trivedi: Where does the data come from to replete potassium to 4 milligrams per deciliter?

Dr. Ben Osher: Pearl 2 – Framework for hypokalemia.

Dr. Shreya Trivedi: What are the 4 big bucket that cause hypokalemia?

Dr. Ben Osher: Pearl 3 – Repletion goals.

Dr. Shreya Trivedi: What is your threshold for potassium repletion, in whom, and how fast?

Dr. Ben Osher: Pearl 4 – Options for hypokalemia treatment.

Dr. Shreya Trivedi: What are the different repletion formulations? And what else can you to do mitigate hypokalemia?

Dr. Ben Osher: Pearl 5 – Frequency of lab checks and repletion.

Dr. Shreya Trivedi: Stepping back, do we really need to get labs every single day?

Pearl 1: Data (or lack thereof) for Potassium Repletion

Dr. Ben Osher: When I started residency, I remember feeling like it was this super important part of my job to make sure that all of my patients had their electrolytes repleted and I would beat myself up if I had forgotten or caught it too late in the day to actually replete. And it got me thinking about why we’re so aggressive about repleting those  potassium levels to 4?

Dr. Shreya Trivedi: Ah! All of that resonates so much and so, Ben, I really appreciate you helping us all pause and dig a little bit deeper into our practices.  

Dr. Ben Osher: So let’s start by trying to get a better idea of what a low potassium on a lab actually means. 

Dr. Shreya Trivedi: Yeah! Great question, because when we’re rounding in the morning and we see that potassium, its flagged as 3.3, how large is that patient’s potassium deficit?

Dr. Melanie Hoenig: When there’s hypokalemia, and I’ll use the official definition of less than 3.5, uh, then there typically is a very significant deficit in potassium. Admittedly, there can be shift into cells that’s transient, say with uh, sudden bout of anxiety and hyperventilation. But otherwise we’re talking about a significant deficit. Because, remember, there’s so much potassium in cells that if there’s a loss of potassium to the body, some of that potassium in cells can simply leak out and provide sufficient potassium in the serum, such that the potassium may look close to normal. So that once we see a clear deficit in potassium in our measurement from the lab, then we’re talking about a very significant deficit. 

Dr. Ben Osher: That was Dr. Melanie Hoenig, a nephrologist at BIDMC and associate professor at Harvard Medical School. 

Dr. Melanie Hoenig: For every one milliequivalent per liter below four, uh, that would reflect a 100 to 200 milliequivalent deficit. And so, uh, there, you’ve got a big task in front of you now because you’re gonna need to replete this. And that estimate doesn’t account for ongoing losses.

Dr. Ben Osher: It’s worth noting that this is variable across patients. Other resources describe even larger deficits of 100 mEq total body K per 0.3 mmol changes in serum potassium. 

Dr. Shreya Trivedi: Yeah, I think either way, the take is that when we do see that low potassium in the chart, that patient has a pretty legit deficit and, to some extent, lost the ability to compensate. And we’ve got some work to do!

Dr. Ben Osher: And speaking of that work, I used to just give patients 10 milliequivalents of potassium for every 0.1 milligrams per deciliter below 4 they are, and forget about it!

Dr. Shreya Trivedi: Forget about it!

Dr. Ben Osher: Yeah! Exactly! Just walk away!  That was until I worked with Dr. Tony Breu at the Boston VA. 

Dr. Tony Breu: One thing that was fascinating to me about the potassium story was that the data that Ben and I discussed when he and I worked together and that many listeners probably seen that was mostly from the eighties, that showed this correlation between a potassium level less than four and increased levels of ventricular arrhythmias. 

Dr. Melanie Hoenig: There is this association, both between problems with low and high potassium, and in particular in patients who are in the post MI period, the post myocardial infarction period, the, or the peri-cardiac surgery period. Those patients do appear to be more ticklish when it comes to hypokalemia. 

Dr. Ben Osher: That really led me down a rabbit hole. So the kicker is that all of these studies from the 80s were done at a time when we didn’t have widespread use of B-blockers and reperfusion therapy was just beginning to be a viable clinical option.

Dr. Shreya Trivedi: Yeah, a very, very different ballgame, indeed!

Dr. Ben Osher: And that’s why researchers re-examined mortality and potassium in patients post-MI in 2012. What they found, as Dr. Hoenig alluded to earlier, is that we do run into potassium problems with levels that are too low or too high, as mortality rates pick up when K was less than 3.5 or greater than 4.5.

Dr. Tony Breu: There’s some data for heart failure that maybe four is better, but again, these are all observational studies.

Dr. Shreya Trivedi: That’s interesting! Hah! So all our practices come from observational data and associations.  

Dr. Ben Osher: I remember feeling so lost so much of the time earlier in intern year, and in a weird way, I took solace in the fact that potassium repletion was something that I could hold onto. I felt like I understood it, I could predict what would happen when I gave someone potassium, I felt like, “well at least I can do this one thing I can fully do on my own that’s helping my patients.”  I was surprised and kind of disappointed  to hear that the evidence for repleting potassium in every patient to 4 milligrams per deciliter is kind of shaky.

Dr. Shreya Trivedi: Yeah, so I’m curious hearing all this, do we have data that repleting potassium actually decreases, then, the risk of those ventricular arrhythmias and mortality?

Dr. Melanie Hoenig: Whether or not re repleting potassium actually decreases that risk, I like to think it does, but I don’t think that’s been well proven.

Dr. Tony Breu: There is no data that I am aware of that if you have a low value by giving potassium back mitigates any risk that comes with that low value, it maybe makes sense for that to be the case. But that doesn’t mean it’s the case. And you do actually need evidence to show that the pathophysiologic mechanisms that we’re invoking bear out.

Dr. Shreya Trivedi: Exactly! Its so surprising we don’t have data to back up repleting potassium and I wonder if it’s just hard study to do given how ingrained repleting potassium is in our clinical practice. 

Dr. Tony Breu: What I found fascinating about the history is not necessarily that, right, that’s just a fact. But the idea that this was quickly incorporated into guidelines for post MI patients, the American Heart Association guidelines. And I think once you have something in a guideline, it is easier for it to be picked up and used more widely. And so the quick incorporation based on this observational data I found surprising. 

Dr. Shreya Trivedi: Yeah, and the other thing worth pointing out in the potassium story, is how repleting to 4 has really even got extrapolated to patients who are NOT post an acute MI, who aren’t post cardiac surgery, who aren’t post acute heart failure actively being diuresed.

Dr. Tony Breu: And then the idea that it hasn’t been explored with as much fervor in non-cardiac patients surprise me given how ubiquitous this practice is. Right? As I’ve said to other people in talking about this, this is an example of indication creep where we have one indication acute MI patients, prevent VT/VF and we say, well if it works for that, let’s do it over here for the patient with pneumonia who doesn’t have a history of cardiac disease. And just, you know, because it works for patient X with condition Y doesn’t mean it’s gonna work for the other patients that you take care of.

Dr. Shreya Trivedi: That indication creep is real! So, I am excited to explore this more. But let’s pause and summarize so far. It sounds like data for potassium repletion really comes from mostly observational studies that correlate a low potassium to ventricular arrhythmias and in-hospital mortality. But this data is really in patients post an acute myocardial infarction and undergoing active diuresis. That being said, we do NOT have evidence to support that repleting potassium to 4 actually prevents adverse events from happening.

Pearl 2: Hypokalemia framework

Dr. Shreya Trivedi: It’s good to know that the data is pretty slim for repletion, but I feel like we are just scratching the surface for our reflexive repletion practices that we do all the time, to potassium of 4. 

Dr. Ben Osher: Yeah, so often we just order that potassium supplement without really thinking why is this person potassium deficient? 

Dr. Tony Breu: But our attention should be diverted away from just buffing the number every day to asking the question why is it low? Even if it’s only mildly low. And I don’t know that we do that enough. I think we’re good at giving potassium, but we’re not necessarily good at asking the question why is it low?

Dr. Shreya Trivedi: Oof! I am so excited to solidify a framework that we can think through when we do see that low potassium pop up.

Dr. Ben Osher: Yeah! So, we can split it into four big buckets. The first is poor oral intake. This is, however, less common. 

Dr. Shreya Trivedi: Yeah! We’re talking here, patients need to have less than 1 g, or 25 mmol, of potassium per day, which as a reference, this is less than 10 dates or 2 avocados a day. 

Dr. Ben Osher: But some of our patients are quite sick, so poor oral intake can certainly be contributing to hypokalemia.

Dr. Shreya Trivedi: Yep! That is very, very valid. So now we get to roll up our sleeves and think about the other 3 big bucket for cause hypokalemia.

Dr. Tony Breu: As with most electrolytes, you can either urinate it out, have it come out through the stool, or it could be shifted into cells.

Dr. Shreya Trivedi: So reiterate one more time, in addition to considering if there is poor potassium intake through food, the 3 other buckets to think about is, is your patient losing potassium through the urine, the stool, or is it being hidden away into cells?

Dr. Tony Breu: For urinary losses, oftentimes we’re doing it to the patient by giving them a diuretic. But you can have RTAs like type one, type two RTA can also cause hypokalemia. 

Dr. Shreya Trivedi: So diuretics cause cause a chloride depletion alkalosis, and usually alkalosis leads to hypokalemia. On the flip side, say you patient has a non-anion gap acidosis and a low potassium, then we start thinking about renal tubular acidosis type 1 or type 2. Or the urinary loss that most people forget about, is that sometimes they are getting too much fluids and maybe that is causing the hypokalemia.

Dr. Melanie Hoenig: Sometimes it can be something as simple as a patient who’s receiving intravenous fluid that does not have potassium in it, let’s just say normal saline. And that with increased distal delivery to the kidney, that will favor losses of potassium in the urine. And, uh, it may be as simple as that. So in that circumstance, maybe you’re just shutting the IV fluid off and letting them eat their normal diet and, uh, they’ll be better tomorrow. 

Dr. Ben Osher: I love that example, because it entails pausing to think what things we’ew giving or maybe doing that are favoring losses of potassium and not just reacting by repleting potassium after the fact. 

Dr. Shreya Trivedi: Yeah! You know, I was surprised to hear that the same mechanism gets invoked when we think about large doses of IV penicillin antibiotics. Those antibiotics increase sodium delivery to the distal nephron and favor potassium loss in the urine.

Dr. Ben Osher: And other things that lead to urine losses of potassium is something else that all of our patients are getting all the time in the hospital or on at home, and those are proton pump inhibitors.

Dr. Tony Breu: Even though you don’t lose the potassium with the PPI, the magnesium that you lose with the PPI also then leads to hypokalemia.

Dr. Shreya Trivedi: Yep and take a look at the infographic that details the urinary causes of potassium loss more and you’ll see an asterisk next to vomiting which most people do think of as a GI cause, but vomiting technically leads to urinary losses of K.

Dr. Melanie Hoenig: One common misconception is that vomiting leads to direct losses of potassium from the vomit. So chronic losses because of vomiting, because of gastroparesis, because of NG suction, those individuals will lose hydrogen chloride. But there’s actually very little potassium in vomit. So here’s what happens. Bear with me! In vomiting, individuals can develop a metabolic alkalosis that can have an excess of bicarbonate in the blood, and if they are not volume depleted, that excess bicarbonate is simply excreted in the urine. We’re really good at getting rid of bicarbonate when we’re not volume depleted. That bicarbonate, when it’s excreted, it doesn’t go out alone. It goes out with the sodium or with the potassium. And so potassium loss, as bicarbonate-uria , bicarbarturia is the reason that individuals who have chronic vomiting develop hypokalemia. 

Dr. Shreya Trivedi: So interesting! Okay, so that’s the pathophys behind vomiting and upper GI tract insults, what about the lower GI tract? How do we lose potassium from below?

Dr. Melanie Hoenig: The key thing is just to recognize that when there’s a lot of movement, a lot of losses of stool, that potassium loss is common. 

Dr. Shreya Trivedi: So, GI losses from below, sounds like basically anything that increases stool volume, whether its diarrhea, laxatives, repeated enemas will lead to fecal loss of potassium. Alright, now let’s move on to last of the 4 buckets lead to hypokalemia, intracellular shifts!

Dr. Tony Breu: And then shifts, and this ends up being really important when we think about all our patients who are in the hospital with a highly adrenergic, acute MI, heart failure, alcohol withdrawal, all these are conditions that are associated with increased epinephrine and that epinephrine is gonna shift potassium into cells. And so sometimes the hypokalemia is a harbinger of the fact that I’m not treating my patient with alcohol use disorder and withdrawal well enough. Right? It’s kind of looking at the heart rate and the blood pressure. Those are indicators of increased catecholamines, well, I think so is hypokalemia!

Dr. Ben Osher: And just to sit with that for a second. So these shifts into cells can happen in highly adrenergic states like an acute MI, alcohol withdrawal, or panic attacks as Dr. Hoenig mentioned earlier, which all activate the sodium/potassium pumps and shift K inside cells. Insulin also acts on those sodium/potassium pumps so you can remember that insulin pushes the K in to cells. 

Dr. Shreya Trivedi: I love that! So catecholamines and insulin are the biggest culprits that often lead to potassium shifts inside cells, and we will link a more comprehensive list in our show notes and infographic. But this may be a good place to pause and summarize, Ben!

Dr. Ben Osher: Yeah, so when we see a low K, we should think of why! Four big questions I now think through when seeing a low K  (1) is the patient not eating enough? (2) is the patient peeing out potassium with a diuretic or do they have an RTA? Or are they peeing it out because they are on fluids or a PPI? (3) Are they losing potassium through stool if they have a lot of diarrhea? Or are they vomiting?

Dr. Shreya Trivedi: And then, lastly, number (4) is there a highly adrenergic state that is causing potassium to shift into cells? And is that a signal for us to get that underlying state under control. And with that, we will leave you with how Dr. Hoenig makes this a little bit fun for herself and thinks about the why!

Dr. Melanie Hoenig: Personally, I love to sort of imagine or postulate what I might see on the labs and, and then you can click it and see the big reveal and see if you’re right. And if the labs have changed as you expected, you’re learning something there. You’re learning what happened when you gave this diuretic and how much the potassium changed or the other electrolytes changed. And if they don’t change at all, you’re learning that. And, and if they change in a way that you didn’t expect, then you have to say, “Well, why did this happen?” And so not that house officers have enough time to, you know, contemplate every single lab study that comes back, but on, on the other hand, that’s part of the fun of it, right? To sort of think about it and, and what the patient experience and why that might happen and apply some basic physiology, uh, right there on the wards or in clinic.

Pearl 3: Goal for K repletion

Dr. Shreya Trivedi: Okay! So now that we delved into the data or lack there for potassium repletion, we have a systematic way to think through the causes of hypokalemia, putting all this together, Ben, I’m curious, how aggressive should we be in trying to get that potassium number back up?

Dr. Ben Osher: I don’t know! The more we talk about this, the more that I’m wondering if I’m helping patients with their homeostasis by giving them potassium, or if I’m treating myself, and making myself feel better about the numbers. 

Dr. Shreya Trivedi: Ugh, that is very honest!

Dr. Tony Breu: The normal range of potassium is three and a half to five. So what that means is that the people who are routinely bringing the potassium to four, are intentionally aiming for a value that isn’t just normal, but is mid-range normal. And I would argue that that’s fairly unique. We don’t do that for hemoglobin, we don’t do that for most electrolytes. We’re not aiming for midrange normal, we’re aiming for low normal. Let’s get them to normal. So with that said, my practice is to aim for three and a half. 

Dr. Shreya Trivedi: I’m just gonna let that sink in, that Dr. Breu is not aiming for that magic 4 number! But then again, it’s not WRONG to aim for 4, especially in certain patient populations. 

Dr. Tony Breu: For heart failure, similar to acute MI, if I have an intern who’s like, let’s get them to four, I have no problem with that. And I often hear the argument because they have continued losses because of our loop diuretics. If they’re 3.5 now, by the time we get to tomorrow they’re gonna be 3.1 or 2.9. I buy that.

Dr. Shreya Trivedi: And the big caveat is that everyone will have their own practice patterns and what makes them feel comfortable.

Dr. Ben Osher: Yeah for me, I’m realizing it can be true both that someone’s full body potassium is a little low and that being a little potassium deficient isn’t really putting them at risk, or causing problems clinically.

Dr. Tony Breu: I’m gonna be careful about how I phrased this cause I’m sure there’s scenarios where a patient has a potassium of 2.6, 2.7 and has a ventricular arrhythmia. But I really think this is one of those two hit hypotheses situations where the hypokalemia alone shouldn’t predispose to a ventricular arrhythmia unless it’s in insanely severe. But even then we see patients who drop to sometimes less than two in there, they don’t have cardiac arrest. You need that second hit, which is a myocardium that is sensitive either because it’s had an MI in their scar or because it’s got a cardiomyopathy, something else that predisposes to the ventricular arrhythmia. And then the hypokalemia is that second hit or whichever order you want to think about it. If they’re less than three, I get nervous and I wanna give them some potassium. But really you have to think about the substrate of that patient and what is that second hit gonna be? In a patient who is young and otherwise healthy and has a potassium of 2.8, I’m not running to the EMR to get it into them. The patient who has just had an acute MI and has clearly high levels of epinephrine, that’s the patient we gotta be a lot more careful about.

Dr. Shreya Trivedi: I love thinking about two hit phenomena. I hadn’t heard it like that before. But I also want the message to be clear that a potassium in the 2s is a pretty significant deficit and clearly something is wrong, but the urgency with which we have replete changes based on the patient and their risk factors.

Dr. Ben Osher: Yeah! So let me try to summarize some of the nuance around this.  Understanding who the patient is can help triage how quickly we need to place the order to replete potassium. 

Dr. Shreya Trivedi: And for spaced repetition from Pearl 1, we are really going to be thinking about those patients who have a risk factor for cardiac arrhythmias, those post an acute MI and those undergoing active diuresis in heart failure. 

Dr. Ben Osher: For those patients who don’t have those cardiac risk factors and are taking in decent PO, my takeaway is to avoid repleting people to 4.0 exactly, and just shoot for normal, like we do with most other things. 

Dr. Shreya Trivedi: Yep! And we will leave you with Dr. Hoenig who gives us some food for thought that this all in the acute setting, but in the long-term low K may not be as great for our patients.  

Dr. Melanie Hoenig: That’s the short term issue. But on the long game is also very provocative, and it appears that having hypokalemia chronically may be an issue for metabolism. And we’re learning more and more that potassium is a beautiful thing and may provide a lot of benefits. I can’t help telling you about this amazing study that was, uh, reported last year in the New England Journal. This was on salt substitute. What they did was they took 600 remote villages in China. And 300 of the villages got a mixture with 25% KCl and 75% sodium chloride. And the other 300 villages just got regular sodium chloride. And at the end of the study, I think it was about, four and a half years, they found that the patients who had had sought substitute had a significantly lower incidence of stroke, major adverse cardiovascular events were death from every, any cause and there was not a significant difference in hyperkalemia. So I found that to be very exciting report and sort of fodder for embracing a high potassium diet. I think that, uh, you know, whether or not you need to replete to a potassium of 4, I don’t feel strongly about that. So thinking about it in the long run I think might make you feel a little bit better about repleting in the short term. If they do have a deficit, then, um, thinking again towards the long game, maybe we’re doing them a favor.

Pearl 4: Potassium repletion

Dr. Ben Osher: So now that we talked about which patients may benefit from potassium repletion versus which patients may not benefit quite as much, this then leads to the question of how we actually go about repleting the patient in front of us.

Dr. Melanie Hoenig: Whenever possible, it’s probably best to use the GI tract, just like we do with nutrition. It’s the safest, and you can tolerate a large amount of potassium over the course of the day. Most people will limit the oral potassium per dose to 40 milli-quivalents, a large amount of potassium. But then you can end up over the course of the day, giving quite a lot in divided doses. 

Dr. Shreya Trivedi: I really appreciate her strategy to give multiple oral doses over the course of day, especially when you contrast that to the IV route, and think about how much potassium you can actually and over how long of a time period.

Dr. Melanie Hoenig: Every hospital has a different protocol for potassium infusion, but a common strategy would be to limit potassium infusion to 10 milli-equivalents per hour. And if anything is given above that, they may require cardiac monitoring. And this would be because transiently the potassium could be higher in the blood and make the prone to arrhythmias.

Dr. Shreya Trivedi: I remember once a I ordered 60 mEq of potassium IV and wondered, “hm, how come it’s taking all afternoon to give?” and the nurse had to kindly educate me on the limits on how mEq can be in a IV bag for a certain the volume. So, my takeaway is to reach, first, for oral potassium, as long as the patient can tolerate it. Sometimes patients do call it a horse pill. And so, with that in mind, lets get into which one of oral potassium options we should choose?

Dr. Melanie Hoenig: When I’m giving potassium supplementations, I also try to think hard about what else they might need. Many patients with hypokalemia have a metabolic alkalosis and so that makes giving potassium chloride particularly attractive as an option. But if they also had a phosphate deficit, you could give potassium phosphate, as an example. Potassium citrate is a favorite for patients who are outpatients and have kidney stones and hypocitruria, low citrate, since citrate is a sort of natural stone inhibitor that chelates calcium. So that would be a reason to choose that.

Dr. Ben Osher: I’m so glad she mentioned this, because potassium chloride is all that most people know, and usually use. But there are different formulations that people can reach for, especially if the phos also low, or if the patient has kidney stones.

Dr. Shreya Trivedi: And speaking of potassium citrate or phosphate, thats the form of potassium that comes in our every day foods. So of course we can ask patients to each more potassium rich foods, like figs, or dried fruits, avocados. More avocados for everybody! But it is hard to predict how much of a bump that we will see with that dietary potassium and absorption. I think we just get too spoiled with the potassium chloride bump that we see all the time when we give it. 

Dr. Ben Osher: So if we are leaning on supplements in the acute setting, what about the dosage? Cause at some point, I was taught that you shouldn’t give more than 60 mEq of oral potassium at any one time.

Dr. Melanie Hoenig: I don’t know where that maximum comes from. I do know that when potassium salts became available in the forties or fifties, sixties, when these interesting experiments were done, very large doses of potassium caused symptoms for patients. When you think about how much you would take and how it can cause GI distress, I think that’s the main issue. I looked for more and I just can’t find where that magic 60 number comes from. I think that may be level C evidence as if, something small, but I think it’s sort of unnecessary.

Dr. Shreya Trivedi: Oh, yeah! I am glad we are calling out hospital policies and things that we get paged about, but maybe don’t have as much backing. But yeah, I do understand, for some patients, if they’re starting to feel a little bit of stomach upset, GI distress with more potassium, we can definitely pump the breaks on that and think about other options .

Dr. Ben Osher: Speaking of other options, Dr. Breu pointed out the importance of looking at the med rec and seeing if we can potentially control the rate of urinary potassium excretion, or kaliuresis, by being selective with our loop diuretics. 

Dr. Tony Breu: Back to this idea of asking why they have hypokalemia instead of just giving, this will sound heretical, but we could probably just give them torsemide, instead of the furosemide, and give it orally cause it’s absorbed wonderfully orally. And guess what? Torsemide doesn’t have nearly as much kaliuresis. The rates of hypokalemia in torsemide are significantly lower than with furosemide. So you’re not gonna need that potassium nearly as much. So if you got a patient you’re giving potassium to every day and they’re on furosemide, consider switching. That’s gonna make things a lot easier for everybody. Torsemide has a aldosterone antagonism effect. Kind of, it almost acts like spironolactone in a way. So as a result, you do get less kaliuresis. In one study the patients on furosemide, like 30% of them were on supplements versus less than 5% on torsemide. I’m not positive about those numbers, but it’s ballpark.

Dr. Ben Osher: Interesting! In that case, it may be worth going with torsemide over furosemide, unless you’re actively attempting to stop someone from becoming hyperkalemic. 

Dr. Shreya Trivedi: Okay so to recap this very short Pearl on potassium repletion, we can be reach potassium chloride, but if there is a phosphate deficit, we can reach for potassium phosphate, or kidney stones, maybe potassium citrate would benefit

Dr. Ben Osher: I’m still so surprised to hear that torsemide causes less hypokalemia than furosemide. Given that both are generic, I’m really going to start reaching for PO torsemide over PO lasix, other things being equal. 

Dr. Shreya Trivedi: And adding things to consider when looking at what meds a patient is on, and some spaced repetition from Pearl 2, we can think about if we can discontinue to that proton pump inhibitor, or think about if its the fluids we are giving them that could be contributing!

 Pearl 5: frequency of lab checks and repletion

Dr. Shreya Trivedi: And so at this point, we’ve explored all things hypokalemia! But what if we take a step back, even further! I feel like each Pearl, Ben, has been one more step back, but, now this is like meta meta! And let’s think about, do we we really need that labs in the first place?

Dr. Melanie Hoenig: We probably order laboratory studies far too often and far too frequently each day on each patient.

Dr. Tony Breu: If you don’t check a potassium, you’re not gonna replete it. I mean that I can assure you.

Dr. Ben Osher: I feel that is some House of God thinking! You can’t find a fever if you don’t check a temperature!

Dr. Shreya Trivedi: Haha! Which is not good, do not reccomend!

Dr. Ben Osher: The other thing that we do, is we check electrolytes twice a day on a patient that we’re actively trying to diurese. Do we really need to do this?

Dr. Melanie Hoenig: So if you start a furosmide infusion and they don’t make a lot of urine, I guarantee you, the potassium’s not gonna change very much. You don’t need labs again later. And the only time you really need labs is if you have a brisk diuresis, and let’s say the potassium was on the low side to start, then it would be reasonable to do labs.

Dr. Tony Breu: If you’ve got a patient who’s generating 4, 5, 6 liters of urine and is consistently having aggressive kaliuresis and they’re hypokalemic, sure check an afternoon potassium. But the number of times I see that afternoon potassium be in the normal range. It’s like, all the time.

Dr. Ben Osher: Shreya, at some level, we all kind of know that we don’t have to order morning labs as part of our daily workflow. But we just keep doing it! Probably in part because sometimes it’s easier to just order the labs, then to expend the brain power to think through why, oh, I maybe don’t need a CBC and I only need electrolytes for this patient.

Dr. Shreya Trivedi: Yeah, I mean, there’s so much inertia from every angle, it’s so hard to stop our everyday practices. 

Dr. Tony Breu: I highly doubt that after decades of this practice, I’m gonna be the guy that gets the intern to stop checking the daily chem seven. What are we gonna talk about in rounds if we don’t have the chem seven?

Dr. Ben Osher: But maybe, we right now, with this podcast, can change this practice! 

Dr. Shreya Trivedi: Oh, man! That would be amazing! We could at least start some conversations. I hope this episode can be inspiring and be sent to everyone’s teams, to nursing colleagues, to pharmacy colleagues, even to the critical lab value people who give us a call for protocolized thresholds for potassium!

Dr. Ben Osher: So maybe instead of morning labs being this daily thing that we check off our to-do list, instead, it might be better to start thinking of ordering a lab as asking a question. We don’t generally check a chest X ray routinely just to make sure that everything’s the same, unless we have some specific reason to think that something may have clinically changed. 

Dr. Tony Breu: I want people to acknowledge that harms of treating do exist. Though I admit that they’re more related to overtreatment and the things that come with this – time, money, inconvenience for the doctor, for the nurse, for the patient. But these things are not insignificant. Right? Time, money, and inconvenience are important.

Dr. Ben Osher: And it’s worth stressing, we can go back and forth all day about whether repleting someone’s potassium to 3.5 or 4 is marginally helping them or not, but it’s worth considering the opportunity cost of doing this.

Dr. Tony Breu: We will make no progress on this. If you believe that we’re maybe overdoing it, we will make no progress if we don’t extend our discussions to include other clinicians. Most specifically nurses. Cause I think a lot of what happens is we teach nurses by our practice that a potassium of 3.3 demands repletion. And so in an attempt to aid us, they will send us a message often via page, “hey, potassium of 3.3.” And an intern who doesn’t feel empowered, is going to give potassium to that patient because they don’t wanna look like they’re dismissive to the nurse, and they don’t want to fail to do something that everyone around them is doing. So unless we engage with everyone who is involved in this practice, we’ll never be able to make any change. The interns are not going to be able to change this practice on their own. Cause they’re going to continue to get pages and they’re gonna continue to have people who say, “Hey, why didn’t you give this patient potassium?” So that the conversation needs to expand. And fortunately for Core IM, I know you guys have a lot of listeners who are not MDs and DOs, but I really hope they hear this message too.

Dr. Ben Osher: I think this is so important! I’m really going to make sure that I understand what’s driving these requests for orders to replete a potassium of, say, 3.7, and if I can avoid boring my colleagues to death, maybe I’ll be able to make a few people a bit more comfortable with a potassium that’s just normal, instead of exactly 4.0.

Dr. Shreya Trivedi: And that’s a wrap for today’s episode. If you found this episode helpful, please share with your team, your colleagues, and give it a rating on Apple podcasts or whatever podcast app you use! It really does help people find us! 

Dr. Ben Osher: If you want to add any of your own tips or share challenges, Tweet us or X- at us and leave a comment on our website page, on instagram or facebook page. 

Dr. Shreya Trivedi: Thank you to our peer reviewer Dr. Jeff William and Dr. Larissa Kruger Gomes. Thank you to Daksh Bhatia for the audio editing. As well as Dr. Vorada Sakulsaengphrapha for the accompanying graphics.  As always we love hearing feedback, email us at hello@coreimpodcast.com. Opinions expressed are our own and do not represent the opinions of any affiliated institutions.

References

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