Whiteboard Animation
Transcript:
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You are on the wards and see a red flag pop up next to potassium in your patient’s morning labs.
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You order a quick 40 mEq dose of potassium chloride, type “replete to 4” in your progress note. But … why do we do this? Why do we care about hypokalemia?
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In this video, we are going to define hypokalemia, talk a little bit about why it’s so important to identify it, then dive into our strategy for correcting it, with either IV or oral potassium repletion.
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So first, what is considered hypokalemia? Hypokalemia is defined as a drop in serum potassium to less than 3.5. A low serum potassium indicates that there is either a total body deficit of potassium or that potassium has shifted into cells.
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We have seen in observation studies that hypokalemia is associated with the increased risk of developing arrhythmias, like VTach. In particular, we see this association in patients with underlying cardiac disease, such as patients who have previous myocardial infarctions, a history of cardiac surgery, and patients undergoing active diuresis.
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Great – Now that you know how to identify hypokalemia, we can move on to the next step, which is correcting it. So how do we know if potassium repletion is indicated for our patients? If patients have no cardiac risk factors, do not have ongoing potassium losses, and are tolerating PO intake, then repleting their potassium is less urgent, especially if they are only mildly hypokalemic or if they are asymptomatic. Instead of medically repleting these patients, you can encourage them to eat potassium rich foods, such as figs, dried fruits, and avocados.
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Our target for repletion should be low-normal, between 3.5 and 4, aiming closer to 4 for patients with higher cardiac risk. And who are our patients with higher cardiac risk again? Patients that are post-acute MI or cardiac surgery, and patients with ongoing losses, like those undergoing active diuresis for heart failure. For these patients repletion is more urgent.
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There are two methods for potassium repletion: IV and PO. PO repletion is preferred unless the patient is unable to take medication by mouth. For example, patients who are vomiting or have dysphagia should be repleted with IV potassium. The same goes for patients who are poor absorbers, like those with an IBD flare or who have undergone bariatric surgery.
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A rule of thumb for repletion is that 10 mEq of potassium increases serum potassium by 0.1 mEq/L. Generally, up to 40-60mEq can be given in one dose, depending on how much a patient can tolerate at one time without causing GI upset.
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If additional repletion is necessary, consider dividing into multiple doses. These doses may be timed to be given after a dose of diuretic. We see this pattern of dosing for our patients who require more frequent diuresis for heart failure, in which case you would expect ongoing losses of potassium.
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For PO potassium, there are several options, depending on your hospital formulary. One of the most common formulations is potassium chloride. Reach for this if your patient has a metabolic alkalosis. Think about patient’s undergoing aggressive diuresis for a HF exacerbation with a resulting contraction alkalosis. If your patient has kidney stones, reach for potassium citrate. Citrate chelates the calcium filtered by the kidneys and prevents stones from forming. This is why we recommend orange juice for patients with recurrent stones, because it contains high levels of citrate. One way to remember why is that the Citrate chelates calcium (what an alliteration!) And if your patient has a phosphate deficit, you can reach for potassium phosphate.
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Now, switching gears quickly to IV potassium. Generally, IV potassium on most hospital formularies is in the form of potassium chloride. It is usually ordered to run at a maximal rate of 10 mEq/hr. Running IV potassium at a slower rate prevents big swings in potassium levels that can put patients at risk for cardiac events. If your patient is severely deficient and you need to be more aggressive with your repletion strategy, be sure to hook them up to telemetry to closely monitor their rhythm. And one more thing to keep in mind is that unfortunately, IV potassium can cause significant pain and discomfort at the infusion site for patients. If your patient is having trouble tolerating this discomfort, try running it at a slower rate, diluting it with normal saline, or applying an ice pack to the site.
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So far we’ve talked a lot about repletion, but that’s only one part of the treatment strategy. If we want to prevent further losses of potassium and not just replace what was lost, we need to take a look at the patient’s med list. Here are some of the common offenders that drive down potassium: Antibiotics, particularly IV penicillin in large doses, and also aminoglycosides and fluoroquinolones. Proton pump inhibitors can also cause hypokalemia, which is driven by magnesium wasting. So protip – If your patient has a low mag and mild hypokalemia, then try repleting their magnesium – this will likely improve the potassium deficiency! The last few meds on our list of common offenders are laxatives, diuretics, and steroids. Exogenous steroids in high doses mimic the action of aldosterone, causing potassium to shift out of cells into the urine. This seems like a lot to remember, so one way to remember a few of these common culprits is the Pesky P’s: where P is for penicillin, PPI, Prednisone (for steroids), Poop (as in laxatives) and Pee (as in diuresis).
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If your patient is hypokalemic and is going to need more diuresis, consider switching from furosemide to torsemide. What’s great about torsemide is that it partially acts as an aldosterone antagonist. So it allows you to get rid of that excess volume your patient is holding on to while minimizing the loss of potassium in the urine! It’s also easy to transition your patients from IV to PO torsemide when they’re getting ready for discharge, because as you can see here, the dose conversion is 1:1!
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When we are giving potassium repletion, we often see twice daily labs, especially for patients who are undergoing diuresis. But are all those repeat BMPs really necessary? The short answer is no, follow-up labs are not always needed. As a rule of thumb, if your patient did not make a ton of urine, with an output of less than 1-2L following a dose of diuretic, then you can assume they won’t be losing much potassium in the urine, and you might not need to recheck labs that day! On the other hand, if your patient did a lot of urine after that diuretic dose, then it might be a good idea to recheck labs more frequently, especially if you plan on diuresing them again!
2 comments on “Potassium Repletion: Whiteboard Animation”
Evidence about K>4:
Is there high-quality evidence about supplementing potassium > 4 mmol/L?
The higher quality trial I know was TIGHT K published last year in JAMA and a more tight supplementation approach wasn’t better.
Great Q! There is more nuance in the episode that goes through the weak data. Observational data that low K levels are associated with higher rates of ventricular arrhythmias in patients who were: post-myocardial infarction, post-cardiac surgery, or undergoing active diuresis in heart failure. However, most of this evidence comes from observational studies decades ago before beta-blockers were widely used. In a 2012 study of patients with acute myocardial infarction had mortality rates lowest in those with a post-admission potassium level between 3.5 and <4.5 mEq/L
Despite these observations, we do not have evidence that repleting serum K leads to better outcomes!