What is the treatment for hyperkalemia?

Treatment of Severe Hyperkalemia (Potassium 7.5 mEq/L)

A potassium of 7.5 mEq/L is a medical emergency requiring immediate multi-pronged treatment: start with IV calcium for cardiac protection, followed simultaneously by insulin/glucose and nebulized albuterol to shift potassium intracellularly, then initiate potassium removal with loop diuretics or hemodialysis depending on renal function. 1

Immediate Assessment (Within Minutes)

• Obtain an ECG immediately to assess for life-threatening cardiac manifestations including peaked T waves, flattened P waves, prolonged PR interval, and widened QRS complex 1, 2
• ECG changes mandate emergency treatment regardless of the exact potassium level, as they indicate imminent risk of fatal arrhythmias 1, 3
• Rule out pseudohyperkalemia from hemolysis or poor phlebotomy technique, but do not delay treatment while waiting for repeat labs if ECG changes are present 1, 2

Step 1: Cardiac Membrane Stabilization (Start Within 1-3 Minutes)

Administer IV calcium first—this is your most urgent intervention: 1, 2

• Calcium gluconate 10%: 15-30 mL (1.5-3 grams) IV over 2-5 minutes 1, 2
• Alternative: Calcium chloride 10%: 5-10 mL (500-1000 mg) IV over 2-5 minutes 1, 2
• Effects begin within 1-3 minutes but last only 30-60 minutes 1
• Critical caveat: Calcium does NOT lower potassium—it only stabilizes cardiac membranes temporarily 1, 2
• Repeat dosing may be necessary if no ECG improvement within 5-10 minutes 1
• Continuous cardiac monitoring is mandatory during and after administration 1

Step 2: Shift Potassium Intracellularly (Start Immediately After Calcium)

Administer all three agents together for maximum effect: 1

Insulin + Glucose (Most Reliable Agent)

• Regular insulin 10 units IV + 25 grams dextrose (50 mL of D50) 1, 2
• Onset: 15-30 minutes, duration: 4-6 hours 1
• Never give insulin without glucose—hypoglycemia can be life-threatening 1
• Monitor glucose closely; patients with low baseline glucose, no diabetes, female sex, and renal dysfunction are at highest risk of hypoglycemia 1
• Can be repeated every 4-6 hours if hyperkalemia persists, with careful monitoring of potassium and glucose every 2-4 hours 1

Nebulized Albuterol

• Albuterol 10-20 mg in 4 mL nebulized over 10 minutes 1, 2
• Onset: 15-30 minutes, duration: 2-4 hours 1
• Use as adjunctive therapy to augment insulin effect 1, 4

Sodium Bicarbonate (ONLY if Metabolic Acidosis Present)

• Sodium bicarbonate 50 mEq IV over 5 minutes ONLY if pH <7.35 or bicarbonate <22 mEq/L 1, 2
• Onset: 30-60 minutes 1
• Do not use without metabolic acidosis—it is ineffective and wastes time 1
• Promotes potassium excretion through increased distal sodium delivery 1

Step 3: Remove Potassium from the Body (Initiate Immediately)

Choose based on renal function and clinical context: 1

If Adequate Kidney Function (eGFR >30 mL/min)

• Furosemide 40-80 mg IV to increase renal potassium excretion 1, 2
• Titrate to maintain euvolemia, not primarily for potassium management 1

If Severe Renal Impairment or Refractory Hyperkalemia

• Hemodialysis is the most effective and reliable method for severe hyperkalemia 1, 5
• Indications: K+ >7.5 mEq/L unresponsive to medical management, oliguria, end-stage renal disease, or ongoing potassium release (tumor lysis, rhabdomyolysis) 1
• Monitor for rebound hyperkalemia 4-6 hours post-dialysis as intracellular potassium redistributes 1

Potassium Binders (Subacute Treatment)

• Sodium zirconium cyclosilicate (SZC/Lokelma): 10 g PO three times daily for 48 hours, then 5-15 g once daily 1
  • Onset: ~1 hour, making it suitable for urgent scenarios 1
• Patiromer (Veltassa): 8.4 g PO once daily with food, titrated up to 25.2 g daily 1
  • Onset: ~7 hours, separate from other oral medications by 3 hours 1
• Avoid sodium polystyrene sulfonate (Kayexalate) due to delayed onset, risk of bowel necrosis, and doubling of serious GI adverse events 1, 6

Step 4: Identify and Address Contributing Factors

Temporarily discontinue or reduce these medications: 1, 3

• RAAS inhibitors (ACE inhibitors, ARBs, mineralocorticoid antagonists) if K+ >6.5 mEq/L 1
• NSAIDs 1, 3
• Potassium-sparing diuretics (spironolactone, amiloride, triamterene) 1
• Trimethoprim, heparin, beta-blockers 1
• Potassium supplements and salt substitutes 1

Assess for underlying causes: 3

• Acute kidney injury, metabolic acidosis, tissue destruction (rhabdomyolysis, tumor lysis) 1, 3
• Adrenal insufficiency, especially in patients with vomiting/diarrhea 7
• Stored blood product transfusion 3

Step 5: Monitoring Protocol

• Check potassium every 2-4 hours initially after treatment 1
• Continuous cardiac monitoring until potassium <6.0 mEq/L and ECG normalizes 1, 3
• Monitor glucose closely to prevent hypoglycemia from insulin 1
• Reassess potassium 7-10 days after any medication adjustments 1

Step 6: Preventing Recurrence

Do not permanently discontinue RAAS inhibitors in patients with cardiovascular disease or proteinuric CKD—they provide mortality benefit: 1, 2

• Once potassium <5.5 mEq/L, restart RAAS inhibitors at lower dose with concurrent potassium binder therapy 1, 3
• Initiate patiromer or SZC to enable continuation of life-saving medications 1
• Target potassium 4.0-5.0 mEq/L to minimize mortality risk 1

Critical Pitfalls to Avoid

• Never delay treatment while waiting for repeat labs if ECG changes are present 1, 2
• Remember that calcium, insulin, and beta-agonists are temporizing measures only—they do NOT remove potassium from the body 1
• Never give insulin without glucose 1
• Never use sodium bicarbonate without metabolic acidosis 1
• Do not rely solely on ECG findings—they are highly variable and less sensitive than laboratory tests 1
• Do not permanently discontinue RAAS inhibitors—use dose reduction plus potassium binders instead 1, 2