Clinical Algorithms

Hyperkalemia Treatment: A Step-by-Step Bedside Guide

DUK-C

October 14, 2026

9 min read

Calcium buys you 30 minutes. It does not lower the potassium. A step-by-step hyperkalemia treatment guide from DUK-C.

The page comes in at 0300: potassium 6.8. The patient is a dialysis patient who missed Saturday's session, or an older man on lisinopril and spironolactone with an AKI, or someone whose sample may simply have hemolyzed. You have a few minutes to decide whether this is a lab artifact or a rhythm about to fall apart.

Hyperkalemia is one of the most common electrolyte emergencies in hospital medicine, and one of the most protocolized. That's exactly why it goes wrong. The order set fires, the insulin goes in, and nobody checks a glucose two hours later. The calcium gets given and everyone relaxes, even though calcium did nothing to the potassium.

Here is the step-by-step version, aligned with KDIGO: confirm it, stratify it, then stabilize, shift, and remove. With doses, timing, and the places where good clinicians still get hurt.

Step 0: Make sure it's real, without waiting to find out

A surprising number of "critical" potassium values are pseudohyperkalemia; potassium released from cells after the blood was drawn. The usual culprits:

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Hemolysis from a difficult draw, a small-gauge needle, or a delayed sample

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Fist clenching or a tourniquet left on longer than a minute

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Marked thrombocytosis or leukocytosis, where cells leak potassium in the tube

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A draw from an arm with a running potassium-containing infusion

The trap runs both ways. If the patient has a plausible reason for true hyperkalemia (renal failure, a missed dialysis session, ACE inhibitors, ARBs, MRAs, trimethoprim, heparin, rhabdomyolysis, tumor lysis, DKA), do not let the word "hemolyzed" talk you out of acting. Get an EKG now, send a repeat (a blood gas analyzer gives you a number in minutes), and treat based on the patient while the redraw is pending. Deciding to wait for the labs is a decision, and in a high-risk patient it is usually the wrong one.

Step 1: Stratify by EKG and trajectory, not the number alone

KDIGO grades hyperkalemia by the number and the EKG together. Mild is 5.0 to 6.0 mEq/L with a normal EKG. Moderate is 6.1 to 6.5 without EKG changes, or 5.0 to 6.0 with them. Severe is above 6.5, or 6.1 to 6.5 with EKG changes. That pairing matters, because the heart responds to how fast potassium rose and what else is going on, not just where it landed.

Treat as an emergency if any of these are true:

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Severe hyperkalemia by KDIGO criteria

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Any EKG change attributable to potassium, at any level

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A rapidly rising potassium (tumor lysis, rhabdomyolysis, crush injury, GI bleed in a renal patient)

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Symptoms: weakness, paresthesias, ascending paralysis, palpitations

The EKG is a warning, not a gauge

The textbook progression goes peaked T waves, then PR prolongation and flattened P waves, then QRS widening, then a sine wave, then VF or asystole. Real patients don't read the textbook. Many people with severe hyperkalemia have a normal-looking EKG, and others jump straight from subtle findings to a wide-complex rhythm or bradyarrest. Look specifically for:

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Tall, narrow, symmetric T waves (most visible in V2 to V4)

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New bradycardia, junctional rhythm, or high-grade AV block

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A QRS that is wider than the last tracing

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A wide, bizarre rhythm that looks like VT but isn't responding the way VT should

If a dialysis patient comes in bradycardic and hypotensive, think hyperkalemia before you think beta-blocker overdose. Pattern recognition here is a skill worth drilling; we cover it in 10 EKG patterns every student and resident should recognize and the EKG mistakes even experienced clinicians make.

Step 2: Stabilize the myocardium with IV calcium

If the EKG shows changes, calcium comes first. It works within 1 to 3 minutes by restoring the gap between resting membrane potential and threshold potential. It does not lower the potassium by a single decimal.

Agent

KDIGO adult dose

Notes

Calcium chloride 10%

10 mL (1 g) IV over 2 to 5 min

About 3x the elemental calcium of gluconate per gram. Vesicant; central line or a large, reliable peripheral IV.

Calcium gluconate 10%

30 mL (3 g) IV, the equivalent dose. Many US order sets give 10 mL (1 g) and repeat.

Peripheral-safe. Preferred when there's no central line.

Three practical points:

Repeat the EKG 5 to 10 minutes after the dose. If the changes persist, give more. Underdosing calcium is a common error. A gram of gluconate carries about a third of the calcium in a gram of chloride, which is why KDIGO's equivalent dose is 30 mL, and why a single 1 g gluconate dose often isn't enough.

The effect wears off in roughly 30 to 60 minutes. Calcium buys time. If potassium-lowering therapy isn't running by then, you have spent that time.

Don't run calcium and sodium bicarbonate through the same line. They precipitate.

On digoxin toxicity: the old "stone heart" teaching that calcium is contraindicated is not well supported by modern data. If digoxin toxicity is driving the potassium, though, the real treatment is digoxin immune Fab, and that should not be delayed.

Step 3: Shift potassium into cells

Shifting buys you hours, not a cure. Total body potassium is unchanged, and it comes back out of the cells once these drugs wear off.

Insulin plus dextrose: the workhorse

Regular insulin IV drives potassium into cells through Na+/K+-ATPase. It starts working in 10 to 20 minutes, peaks around 30 to 60, and typically drops serum potassium by about 0.5 to 1.0 mEq/L.

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Standard dose: regular insulin 10 units IV with 25 g dextrose (50 mL of D50, or 250 mL of D10).

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Reduced dose: 5 units, or 0.1 units/kg, for patients at high risk of hypoglycemia. That means advanced CKD or dialysis dependence, low body weight, no diabetes, older age, or a low-normal starting glucose.

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Skip the dextrose only if glucose is above 200 mg/dL (the KDIGO threshold), and still monitor.

The dose debate is real. In a large cohort of patients with renal insufficiency, 5 units lowered potassium as much as 10 units, with hypoglycemia in 19.5% versus 28.6%. A meta-analysis found reduced dosing roughly halved the odds of hypoglycemia. But at least one study in moderate CKD found 10 units lowered potassium more (0.9 vs 0.63 mEq/L) without a hypoglycemia difference. The fair reading: reduced dosing is reasonable in high-risk patients, and it may need repeating sooner.

The hypoglycemia is late. Insulin outlasts the dextrose bolus; lows cluster around 1 to 3 hours and can occur out to 6. Check glucose at least hourly for the first 4 to 6 hours. In high-risk patients or anyone starting with a low-normal glucose, a dextrose infusion after the bolus is a reasonable safeguard. This is the step most often missed, usually because the patient is boarding in the ED or between handoffs.

Nebulized albuterol: the add-on

Albuterol 10 to 20 mg nebulized (four to eight times the bronchodilator dose) shifts potassium within about 30 minutes and is additive to insulin. Use it together with insulin, not instead of it; a meaningful minority of patients, especially on dialysis or beta-blockers, barely respond. Use caution with active ischemia or tachyarrhythmias.

Sodium bicarbonate: only for acidosis

Bicarbonate is a weak, inconsistent potassium shifter on its own. KDIGO suggests it only for patients with metabolic acidemia (work it up with an anion gap). It is not a stand-alone hyperkalemia treatment, and it carries a sodium and volume load that dialysis patients often can't afford.

Step 4: Remove potassium from the body

This is the step that actually fixes the problem. There are only three exits: the gut, the kidneys, and the dialyzer.

Potassium binders

Binder

Typical acute dose

Onset

Watch for

Sodium zirconium cyclosilicate (Lokelma)

10 g PO TID for up to 48 hours

About 1 hour

Edema from the sodium load; separate other oral meds by 2 hours

Patiromer (Veltassa)

Not advised acutely; 8.4 g PO daily for chronic use

About 7 hours

Hypomagnesemia, constipation; separate other oral meds by 3 hours

Sodium polystyrene sulfonate (Kayexalate)

15 to 60 g PO or PR, never with sorbitol

Slow and unpredictable

Intestinal necrosis (FDA warning); little acute benefit

KDIGO's emergency department guidance favors sodium zirconium cyclosilicate, calls patiromer not advisable for acute treatment because of its 7-hour onset, and keeps sodium polystyrene sulfonate only as an option given without sorbitol. Kayexalate still lives in a lot of order sets out of habit. If yours offers sodium zirconium cyclosilicate, that is the faster and better-studied choice. None of these replace dialysis in a patient who needs it.

Kidneys

If the patient makes urine, use it. A loop diuretic (for example, furosemide 40 to 80 mg IV, more in CKD) helps the volume-overloaded patient. Isotonic fluids help the dry patient with prerenal AKI. Neither does much in oliguric renal failure.

Dialysis

Hemodialysis is the definitive treatment, and the call should come early, not after the third round of insulin. Get nephrology on the phone in parallel with medical therapy for:

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Any patient on maintenance dialysis (KDIGO recommends nephrology involvement for all of them), especially after a missed session

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Severe hyperkalemia refractory to initial therapy

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Oliguric AKI

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Ongoing potassium release (rhabdomyolysis, tumor lysis)

Step 5: Monitor, expect the rebound, and find the cause

The second potassium is where cases go sideways. Shift therapy fades over the next few hours, and the potassium that was hiding in cells walks back out; KDIGO notes rebound can start at 2 to 3 hours if nothing has removed it from the body.

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Recheck potassium at 60 minutes, again at 2 to 4 hours, and at 24 hours. Repeat the shift therapy if it climbs back.

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Check glucose hourly for at least 4 to 6 hours after any insulin dose.

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Keep the patient on a monitor until the potassium is falling and the EKG has normalized.

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Stop the contributors: potassium supplements and potassium-containing fluids, ACE inhibitors, ARBs, MRAs, NSAIDs, trimethoprim, heparin, and potassium-based salt substitutes at home.

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Name the mechanism before the patient leaves: intake, impaired excretion, or a shift. The answer decides whether this happens again next week.

The 30-second version

Real? Repeat the sample, but don't wait if the patient is high risk.

EKG changes or severe hyperkalemia? IV calcium now, repeat EKG in 5 to 10 minutes.

Shift: insulin (5 to 10 units) plus dextrose, plus nebulized albuterol 10 to 20 mg.

Remove: binder, diuretic or fluids, and call nephrology early.

Monitor: glucose hourly, potassium at 1 hour, 2 to 4 hours, and 24 hours. Fix the cause.

Four mistakes that still hurt patients

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Treating the calcium as the treatment. Calcium protects the heart for less than an hour. The potassium is unchanged.

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Giving insulin and walking away. The hypoglycemia shows up hours later, often after handoff.

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Trusting a normal EKG. It is insensitive. A normal tracing does not make a potassium of 7 safe.

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Celebrating the first recheck. A good number at 1 hour says the shift worked, not that the problem is solved. Recheck at 2 to 4 hours.

The takeaway

Hyperkalemia management is simple on paper: stabilize, shift, remove. The harm comes from the gaps between those steps; the calcium that wasn't repeated, the glucose nobody checked, the dialysis call made three hours late. A good protocol isn't one you've memorized. It's one you can pull up and follow completely at 0300, including the parts that happen after you've stopped watching.

Why we built DUK-C around moments like this

We built DUK-C because the right answer usually exists; it's just buried in a 40-page PDF when you need it in 30 seconds. The hyperkalemia protocol in DUK-C lays out the same stabilize, shift, remove sequence with doses, monitoring, and escalation points, sourced to the guidelines behind them. The protocol library is free.

If you want to sharpen the EKG side, the EKG Interpretation Center includes an Electrolyte Abnormalities category with quiz mode, and Patient Context Mode lets you work through protocols with your actual patient's details in front of you. Both are part of a one-time premium unlock.

Less searching. More medicine. The hyperkalemia protocol and the full DUK-C protocol library are free at dukc.app.

References

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Clase CM, et al. Potassium homeostasis and management of dyskalemia in kidney diseases: conclusions from a KDIGO Controversies Conference. Kidney Int. 2020;97(1):42-61.

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Lindner G, et al. Acute hyperkalemia in the emergency department: a summary from a KDIGO conference. Eur J Emerg Med. 2020;27(5):329-337.

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ACEP. Management Algorithm for Adults with Hyperkalemia.

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Comparison of 5 versus 10 units of insulin for hyperkalemia in patients with renal insufficiency. Pharmacotherapy. 2017.

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Alternative insulin dosing for hyperkalemia: a meta-analysis of effects on hypoglycemia and potassium reduction. Pharmacotherapy. 2021.

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5 versus 10 units of IV insulin for hyperkalemia in moderate renal dysfunction. University of Maryland Emergency Medicine.

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Sodium polystyrene sulfonate, patiromer, and sodium zirconium cyclosilicate: pharmacologic comparison. Kidney Int. 2018.

Doses reflect common adult practice and KDIGO conference guidance; follow your institution's protocol.

Frequently Asked Questions

What is the first-line treatment for hyperkalemia?

If there are EKG changes or hyperkalemia is severe, give IV calcium first to stabilize the myocardium. Then shift potassium into cells with IV insulin plus dextrose and nebulized albuterol, and remove it with a binder, diuresis, or dialysis.

How much insulin do you give for hyperkalemia?

Regular insulin 10 units IV with 25 g of dextrose is the traditional dose. Many institutions use 5 units (or 0.1 units/kg) for patients at high risk of hypoglycemia, such as those with advanced CKD or dialysis dependence, low body weight, or no diabetes.

What is the calcium gluconate dose for hyperkalemia?

KDIGO's dose is 10 mL of 10% calcium chloride over 2 to 5 minutes, or the equivalent 30 mL (3 g) of 10% calcium gluconate. Many US order sets give 1 g of gluconate and repeat it. Repeat the EKG 5 to 10 minutes after each dose and give more if changes persist.

Does calcium lower potassium?

No. IV calcium stabilizes the cardiac membrane within minutes but does not change serum potassium. Its effect lasts roughly 30 to 60 minutes, so potassium-lowering therapy must start at the same time.

Is a normal EKG reassuring in hyperkalemia?

No. The EKG is insensitive, and changes don't progress in a predictable order. Patients can deteriorate to a wide-complex rhythm or arrest without passing through peaked T waves first.

Should Kayexalate be used for acute hyperkalemia?

Only if nothing better is available. Sodium polystyrene sulfonate has a slow, unpredictable onset and carries an FDA warning for intestinal necrosis. KDIGO's emergency department guidance favors sodium zirconium cyclosilicate for acute use; if Kayexalate is used, it should never be given with sorbitol.

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