What is the treatment for hyperkalemia?

Treatment of Hyperkalemia

For severe hyperkalemia (≥6.5 mEq/L) or any level with ECG changes, immediately administer IV calcium for cardiac membrane stabilization, followed by insulin with glucose and nebulized albuterol to shift potassium intracellularly, then initiate definitive potassium removal with loop diuretics or hemodialysis. 1

Severity Classification and Initial Assessment

• Mild hyperkalemia: 5.0-5.9 mEq/L 1, 2
• Moderate hyperkalemia: 6.0-6.4 mEq/L 1, 2
• Severe hyperkalemia: ≥6.5 mEq/L (life-threatening) 1
• ECG changes indicating urgent treatment regardless of potassium level: peaked T waves, flattened P waves, prolonged PR interval, widened QRS 1, 2
• Exclude pseudohyperkalemia from hemolysis, repeated fist clenching, or poor phlebotomy technique before initiating aggressive treatment 1, 2

Acute Management Algorithm (Severe Hyperkalemia or ECG Changes)

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

• Calcium chloride 10%: 5-10 mL (500-1000 mg) IV over 2-5 minutes (preferred for rapid effect) 1, 2
• Alternative: Calcium gluconate 10%: 15-30 mL IV over 2-5 minutes 1, 2
• Onset: 1-3 minutes; Duration: 30-60 minutes 1, 2
• Critical caveat: Calcium does NOT lower serum potassium—it only protects against arrhythmias 1, 2
• Administration warning: Use central venous catheter when possible; peripheral extravasation causes severe tissue injury 1
• Monitor heart rate during infusion and stop if symptomatic bradycardia occurs 1

Step 2: Shift Potassium Intracellularly (Onset 15-30 Minutes, Duration 4-6 Hours)

• Insulin with glucose: 10 units regular insulin IV with 25g glucose (50 mL D50W) over 15-30 minutes 1, 2

  • Can be repeated every 4-6 hours if hyperkalemia persists, with careful glucose monitoring 2
  • High-risk for hypoglycemia: low baseline glucose, no diabetes, female sex, altered renal function 2
  • Do not administer if potassium <3.3 mEq/L 2

• Nebulized albuterol: 10-20 mg over 15 minutes 1, 2

  • Onset: 15-30 minutes; Duration: 2-4 hours 1, 2
  • Use as adjunctive therapy with insulin/glucose 2

• Sodium bicarbonate: 50 mEq IV over 5 minutes 1

  • ONLY use if concurrent metabolic acidosis present (pH <7.35, bicarbonate <22 mEq/L) 1, 2
  • Onset: 30-60 minutes (slower than other agents) 2
  • Common pitfall: Do NOT use in patients without acidosis—it is ineffective and potentially harmful 2

Step 3: Eliminate Potassium from Body (Definitive Treatment)

• Loop diuretics: Furosemide 40-80 mg IV 1, 2

  • Only effective in patients with adequate renal function 1, 2
  • Mechanism: Increases urinary potassium excretion 2

• Hemodialysis 1, 2

  • Most reliable and effective method for severe hyperkalemia 1, 2
  • Indications: Severe cases unresponsive to medical management, oliguria, end-stage renal disease, renal failure 2, 3

• Cation exchange resins (NOT for acute management):

  • Sodium polystyrene sulfonate (Kayexalate): 15-50 g orally or rectally 1
  • FDA limitation: Should NOT be used as emergency treatment due to delayed onset of action 4
  • Serious warning: Risk of intestinal necrosis, bowel perforation, ischemic colitis—avoid concomitant sorbitol 5, 4
  • Chronic use should be avoided due to severe gastrointestinal side effects 5

Chronic/Recurrent Hyperkalemia Management

For Patients on RAAS Inhibitors (ACE Inhibitors, ARBs, MRAs)

The priority is maintaining life-saving RAAS inhibitor therapy while managing hyperkalemia with potassium binders, rather than discontinuing these medications. 5, 1, 2

Potassium 5.0-6.5 mEq/L:

• Initiate approved potassium-lowering agent immediately 5, 1, 2
• Maintain RAAS inhibitor therapy unless alternative treatable cause identified 5, 1, 2
• Monitor potassium levels closely 5, 1

Potassium >6.5 mEq/L:

• Temporarily discontinue or reduce RAAS inhibitor dose 5, 1, 2
• Initiate potassium-lowering agent when levels >5.0 mEq/L 1, 2
• Carefully reintroduce RAAS inhibitors as soon as possible while monitoring potassium 5

Newer Potassium Binders (Preferred for Long-Term Management)

• Sodium zirconium cyclosilicate (SZC/Lokelma): 2, 6

  • Dosing: 10 g three times daily for 48 hours, then 5-15 g once daily for maintenance 2
  • Onset: ~1 hour (fastest acting) 2
  • FDA limitation: Not for emergency treatment of life-threatening hyperkalemia 6

• Patiromer (Veltassa): 2

  • Dosing: Start 8.4 g once daily, titrate up to 25.2 g daily based on potassium levels 2
  • Onset: ~7 hours 2
  • Administration: At least 3 hours before or after other oral medications 2

• Advantages over traditional resins: Safer, better tolerated, no risk of bowel necrosis, enable continuation of RAAS inhibitors 5, 7, 8

Additional Chronic Management Strategies

• Eliminate contributing medications: NSAIDs, trimethoprim, heparin, beta-blockers, potassium supplements, salt substitutes 2
• Optimize diuretic therapy: Loop or thiazide diuretics to increase urinary potassium excretion 5, 2
• Dietary modification: Evidence linking dietary potassium to serum levels is limited; potassium-rich diet has cardiovascular benefits including blood pressure reduction 2

Monitoring Protocol

• Check potassium within 1 week of starting or escalating RAAS inhibitors 5, 2
• Reassess 7-10 days after initiating potassium binder therapy or dose changes 5, 2
• More frequent monitoring required in high-risk patients: CKD, heart failure, diabetes, history of hyperkalemia 2
• Monitor every 2-4 hours after initial acute treatment with insulin/glucose 2

Critical Pitfalls to Avoid

• Do not rely solely on ECG findings—they are highly variable and less sensitive than laboratory tests 2
• Remember that calcium, insulin, and beta-agonists are temporizing measures only—they do NOT remove potassium from the body 1, 2
• Rebound hyperkalemia can occur after 2 hours with temporary measures; initiate definitive potassium removal early 1
• Always administer glucose with insulin to prevent hypoglycemia 1, 2
• Avoid sodium polystyrene sulfonate for acute management due to delayed onset and serious gastrointestinal risks 5, 4
• Do not discontinue RAAS inhibitors prematurely in cardiovascular disease or proteinuric CKD—use potassium binders instead 5, 1, 2