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Chapter 5

Evidence Based Hyperkalemia Management

Rob Orman, MD and Britt Long, MD

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Hyperkalemia is one of, if not the most, common electrolyte abnormalities we see. But much of what we do in treatment is what someone told us to do when we were young learners. In this episode we debunk hyperkalemia myths and discuss an evidence based approach to management


  • Dysrhythmias are associated with both the absolute value of potassium and its rate of rise.

  • ECG changes associated with adverse cardiac events include QRS prolongation, HR <50, and a junctional rhythm.

  • Long treats hyperkalemia if serum K ≥ 6.5 or if there are any ECG changes.

  • Calcium will work within 2-3 minutes to stabilize the myocardium.  Redose if no ECG improvement is seen.

  • The onset of action of insulin for hyperK is within 15 minutes and it can last 90 minutes.  Reduce the dose in the setting of renal failure.

  • There is insufficient evidence that Kayexalate is helpful in treating hyperK (but  data that it is harmful.)

  • Since 90% of potassium is renally excreted, diuresis is a viable option for elimination, especially if the patient is hyper- or euvolemic.

  • Note: Potassium is measured as mEq/L in US customary units and mmol/L in SI units, but there is a 1:1 conversion factor.. For example, 4 mEq/L converts to 4 mmol/L



  • Hyperkalemia is likely the most common actionable life-threatening electrolyte abnormality that we see.  It can be broken down into several categories:  mild (K>5.5), moderate (K>6.5) and severe (K>7.5).

  • Factitious hyperkalemia should be suspected if an elevated potassium level doesn’t fit the patient’s clinical picture.  This is due to the release of potassium from lysed blood cells, often due to poor phlebotomy technique.  If the finding of hyperkalemia doesn’t make sense, repeat the lab to determine if it’s real.

  • When should we start worrying about hyperkalemia?

    • Potassium at high levels causes membance instability and cardiac dysrhythmias.

      • The classic teaching has been of a progression of ECG changes starting with peaked T waves→ QT interval shortening→ PR prolongation,→ P wave decrease→ QRS widening→ sine wave.   The problem is that the EKG doesn’t always follow this progression.

      • A recent study looked at which cardiac rhythms were associated with adverse events in hyperkalemia.  

        • This was a retrospective study of 188 patients with K ≥ 6.5.  Adverse events within 6 hours were symptomatic bradycardia, V-tach, V-fib, CPR and/or death.  

        • 15% of the hyperkalemia patients had an adverse event, and all of these patients had one of three ECG changes:  QRS prolongation, bradycardia <50 bpm, and a junctional rhythm. Peaked T waves did not correlate with immediate bad outcomes.  

        • Durfey, Nicole, et al. "Severe hyperkalemia: Can the electrocardiogram risk stratify for short-term adverse events?." Western Journal of Emergency Medicine 18.5 (2017): 963. PMID: 28874951

      • Cardiac instability is associated with not only the absolute level of serum potassium, but even more importantly with the rate of increase of the potassium level.

    • Long starts treatment for hyperkalemia if serum K > 6.5 or if there are any ECG changes (including peaked T waves).  

  • There are 3 goals for the management of hyperkalemia.

    • Stabilize the cardiac cellular membrane.

      • Calcium is the primary treatment to protect against dysrhythmias.

      • Calcium chloride has 3 times the amount of calcium compared with the same volume of calcium gluconate (13.6 meq vs 4.6 meq).  The problem with calcium chloride is that it’s irritating at the injection site and extravasation can result in tissue necrosis.

      • Common practice is to give a gram of calcium gluconate it you’re giving it through a peripheral IV, but give calcium chloride if the patient is in arrest or you have central access.

      • Both forms of calcium have a similar onset of action.  Within 2-3 minutes post infusion, you should see improvement on the monitor or ECG.  If he sees no change after the first amp of calcium, Long keeps redosing until he does.  What he is looking for is narrowing of the QRS.

    • Shift or redistribute the extracellular potassium into cells.

      • Insulin recruits specific channels in the cell membrane which causes cellular uptake of potassium.

        • The classic dosing is 10 units of regular insulin with 1 amp of D50 or 25 grams of dextrose.  This dose will decrease serum potassium by 0.6-1.2 mmol/L within 1 hour; the onset of action is 5 to 15 minutes.

        • For patients with a normally functioning renal system, the effect will last from 90 minutes to 2 hours.  In the setting of kidney failure, it can last much longer.

        • Short-acting synthetic insulins have a theoretical advantage over regular insulin for patients with ESRD.  In addition to having a very short half-life, they are not renally excreted. The literature suggests that they have a similar decrease in serum potassium compared with regular insulin and that they have a reduced risk of hypoglycemia.  Unfortunately, there is not yet enough data to support a definitive dosing regimen.

        • For patients with renal failure or a creatinine clearance under 30, a common strategy is to give a lower dose of regular insulin (ie. 5 units) in an effort to reduce the risk of hypoglycemia.  

          • McNicholas, Bairbre A., et al. "Treatment of hyperkalemia with a low-dose insulin protocol is effective and results in reduced hypoglycemia." Kidney international reports 3.2 (2018): 328-336.PMID: 29725636 Full Text

        • When treating with insulin, you need to anticipate hypoglycemia and give dextrose if the blood sugar is less than 250.   Since the hypoglycemic effects of IV insulin last longer than a bolus of dextrose, often more than 1 amp of D50 is necessary.  The following protocol has been suggested:

          • If the glucose is over 250, don’t give any glucose.  

          • If below 250, give an amp of D50 and recheck the sugar every 30 minutes for an hour and then again 1 hour later.

      • Beta-agonists, such as albuterol, can result in serum potassium redistribution into the cell.  

        • Albuterol can be given by nebulization, subcutaneous, or IV route.

        • If nebulized, the dose is 10-20 mg of albuterol (much higher than the 2.5 mg in a Duoneb). The literature states that this dose can decrease serum potassium by 0.6 mmol within 30 minutes.

      • Sodium bicarbonate works by alkalinizing the serum, redistributing potassium through ion channels.  It may also have a dilutional effect.

        • The problem with studies of bicarb is that most have looked at continuous infusion rather than bolus dosing.  The little evidence that does support bicarb use is in patients with metabolic acidemia.

        • The onset of action is up to a few hours, depending on how it’s given.

        • Long gives an amp of bicarb if a hyperkalemic patient’s venous blood gas shows metabolic acidosis or if a patient is in cardiac arrest.  An article he authored states: “Bicarbonate does not result in a significant decrease in serum potassium when the pH is normal, but it may have benefit in the patient with metabolic acidemia.”

        • Long, Brit, Justin R. Warix, and Alex Koyfman. "Controversies in Management of Hyperkalemia." The Journal of emergency medicine (2018).

    • Eliminate or excrete the potassium from the body.

      • Although Kayexalate is commonly given in the hopes that it will facilitate potassium excretion, there is really no good evidence that it works and it can have deleterious effects.  Furthermore, only 10% of potassium is excreted in the GI system.

        • Kayexalate is an ion exchange resin that exchanges sodium for other ions, such as potassium.  The theory is that Kayexalate would target potassium elimination through the feces.

        • Studies looking at the effect of Kayexalate on potassium levels have not shown benefit.  

        • Adverse side effects include severe constipation and potentially obstruction.  To counter these effects, it is typically dosed with an osmotic cathartic such as sorbitol.  But when provided together, there is an increased risk of colonic necrosis and death. The FDA issued a warning against the use of Kayexalate for this reason.

        • The Journal of the American Society of Nephrology says, “It would be wise to exhaust all other alternatives for managing hyperkalemia before turning to these largely unproven and potentially harmful therapies.”

        • Sterns, Richard H., et al. "Ion-exchange resins for the treatment of hyperkalemia: are they safe and effective?." Journal of the American Society of Nephrology (2010): ASN-2010010079.PMID: 20167700

      • Since 90% of potassium is renally excreted, diuresis is a viable option for elimination, especially if the patient is hyper- or euvolemic and has normal renal function.

        • A loop diuretic, such as furosemide, will have the greatest effect on renal excretion.  Long gives 20-40 mg.

        • Adding acetazolamide or a thiazide diuretic can have synergistic effects, but you have to closely monitor the urine output and electrolytes due to the high risk of hypovolemia and volume contraction.

        • If the patient is dehydrated, you will need to give IV fluids prior to diuresis to reduce their contraction alkalosis.  Long favors the use of Ringer’s lactate since saline can cause acidemia which actually worsens serum potassium levels.

      • Patiromer is a synthetic polymer that exchanges calcium for potassium in the distal colon and can increase GI excretion of potassium.  It will not have an effect for at least 7 hours and is considered a “fringe” medication.

      • ZS-9 is a non-absorbable selective cation exchanger that is highly selective for potassium and ammonium.  Unlike Kayexalate, it doesn’t have the high risk of colonic necrosis.

      • Hemodialysis is the most efficacious means of removing potassium from the body.  You can decrease potassium by 1 mmol/L within the first hour and another 2 mmol/L within 2-3 hours.

        • Indications for dialysis:  known or established renal failure, oliguric acute renal injury, creatinine clearance < 30 with a K greater than 6.5 or ECG changes, production of less than 400 ml of urine per day, failure of other treatments, cardiac arrest, and marked tissue obstruction (such as severe rhabdo).

  • What should be your next step, if a hyperkalemic patient goes into cardiac arrest after you’ve already given calcium, insulin, a beta agonist, and diuretics?  

    • Epinephrine -- The intrinsic beta agonist effects of epi can cause cellular redistribution of potassium.  Give it every 3-5 minutes per ACLS protocol.

    • Dialysis -- There are case reports that have demonstrated successful return of spontaneous circulation and neurologic outcomes by pairing dialysis with CPR.

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