How to treat hyperkalemia?

Treatment of Hyperkalemia at 6.2 mEq/L

For a potassium level of 6.2 mEq/L, you should obtain an immediate ECG and if ECG changes are present (peaked T waves, widened QRS, prolonged PR interval), administer intravenous calcium gluconate 15-30 mL of 10% solution over 2-5 minutes for cardiac membrane stabilization, followed by insulin 10 units IV with 25 grams of dextrose and nebulized albuterol 20 mg to shift potassium intracellularly, then initiate potassium removal with newer potassium binders (patiromer or sodium zirconium cyclosilicate) rather than sodium polystyrene sulfonate. 1, 2

Immediate Assessment and Risk Stratification

• Obtain an ECG immediately to assess for life-threatening cardiac effects including peaked T waves, flattened P waves, prolonged PR interval, or widened QRS complex 1, 2
• Verify this is not pseudohyperkalemia by confirming proper blood sampling technique without hemolysis or prolonged tourniquet application 1, 2
• At 6.2 mEq/L, this falls into the severe category (>6.0 mEq/L) by European Society of Cardiology criteria and requires urgent treatment 1

Acute Management Protocol

Step 1: Cardiac Membrane Stabilization (if ECG changes present)

• Administer calcium gluconate 10% solution: 15-30 mL IV over 2-5 minutes (or calcium chloride 10%: 5-10 mL IV over 2-5 minutes if central access available) 2
• Effects begin within 1-3 minutes but last only 30-60 minutes and do not lower total body potassium 2
• Repeat dosing may be necessary if no ECG improvement within 5-10 minutes 2
• Maintain continuous cardiac monitoring during and after administration 2

Step 2: Shift Potassium Intracellularly

• Insulin with glucose: Administer 10 units regular insulin IV with 25 grams dextrose (50 mL of D50W) 1, 2

  • Onset of action: 15-30 minutes
  • Duration: 4-6 hours
  • Monitor glucose closely to prevent hypoglycemia 2
  • Can be repeated every 4-6 hours if hyperkalemia persists 2

• Nebulized albuterol: 20 mg in 4 mL nebulized as adjunctive therapy 1, 2

  • Onset: 30 minutes
  • Duration: 2-4 hours
  • Use in combination with insulin for additive effect 2

• Sodium bicarbonate: ONLY if concurrent metabolic acidosis present (pH <7.35, bicarbonate <22 mEq/L) 1, 2

  • Onset: 30-60 minutes
  • Do NOT use routinely without acidosis 2

Step 3: Remove Potassium from the Body

Preferred approach: Newer potassium binders 3, 1, 2

• Sodium zirconium cyclosilicate (SZC/Lokelma): 10 g orally three times daily for 48 hours, then 5-15 g once daily for maintenance 3, 2

  • Onset of action: 1 hour (fastest available)
  • Highly selective for potassium
  • Works in small and large intestines 3

• Patiromer (Veltassa): 8.4 g orally once daily, titrate up to 25.2 g daily based on response 3, 2

  • Onset of action: ~7 hours
  • Administer at least 3 hours before or after other oral medications 3

Avoid sodium polystyrene sulfonate (Kayexalate): This agent has delayed onset of action, is not appropriate for emergency treatment, and carries significant risk of intestinal necrosis and bowel perforation, particularly when used with sorbitol 1, 4

Step 4: Enhance Renal Excretion (if adequate kidney function)

• Loop diuretics: Furosemide 40-80 mg IV if eGFR >30 mL/min/1.73m² 1, 2
• Titrate to maintain euvolemia, not primarily for potassium management 2

Step 5: Consider Hemodialysis

• Reserve for severe cases unresponsive to medical management, oliguria, or end-stage renal disease 1, 2
• Most reliable and effective method for potassium removal 2, 5

Medication Management

RAAS Inhibitor Adjustment

• At K+ 6.2 mEq/L, temporarily reduce or hold RAAS inhibitors (ACE inhibitors, ARBs, mineralocorticoid receptor antagonists) 3, 1
• Do NOT discontinue permanently—these provide mortality benefit in cardiovascular and renal disease 1, 2
• Once potassium decreases to <5.0 mEq/L and any concurrent contributing condition is controlled, reinitiate RAAS therapy at lower dose with concurrent potassium binder 3, 1
• Reintroduce agents one at a time with close monitoring 3

Eliminate Contributing Medications

• Stop or reduce: NSAIDs, trimethoprim, heparin, potassium-sparing diuretics, potassium supplements, salt substitutes 1, 2

Monitoring Protocol

• Check potassium every 2-4 hours initially after acute interventions 2
• Recheck within 24-48 hours to assess response 1
• Once stabilized on potassium binder, reassess at 7-10 days, then 1-2 weeks, 3 months, then every 6 months 2
• Monitor for hypokalemia with chronic binder therapy, as this may be more dangerous than mild hyperkalemia 2

Dietary Modifications

• Restrict potassium intake to <3 g/day (50-70 mmol/day) 1
• Avoid high-potassium foods: bananas, oranges, melons, potatoes, tomato products, legumes, lentils, chocolate, yogurt 1
• Eliminate salt substitutes containing potassium 1

Critical Pitfalls to Avoid

• Do not rely solely on ECG findings—they are variable and less sensitive than laboratory values 2
• Do not use sodium bicarbonate without metabolic acidosis—it is only indicated when acidosis is present 1, 2
• Remember that calcium, insulin, and beta-agonists are temporizing measures only—they do not remove potassium from the body 2
• Always administer glucose with insulin to prevent life-threatening hypoglycemia 2
• Do not permanently discontinue RAAS inhibitors—use potassium binders to maintain these life-saving medications 1, 2
• Avoid sodium polystyrene sulfonate for acute management due to delayed onset and serious gastrointestinal risks including bowel necrosis 1, 4

Special Considerations for CKD Patients

• Optimal potassium range is broader in advanced CKD: 3.3-5.5 mEq/L for stage 4-5 CKD 2
• Maintain RAAS inhibitors aggressively in proteinuric CKD using potassium binders, as these drugs slow CKD progression 2
• Target potassium of 4.0-5.0 mEq/L minimizes mortality risk 2