What are the steps for managing hyperkalemia?

Management of Hyperkalemia

Hyperkalemia management follows a severity-based algorithmic approach: immediate cardiac membrane stabilization with IV calcium for severe cases or ECG changes, followed by intracellular potassium shifting with insulin/glucose, and finally total body potassium elimination through diuretics, newer potassium binders, or dialysis. 1

Severity Classification

• Mild hyperkalemia: K+ >5.0 to <5.5 mEq/L 1
• Moderate hyperkalemia: K+ 5.5 to 6.0 mEq/L 1
• Severe hyperkalemia: K+ >6.0 mEq/L (life-threatening) 1

The presence of ECG changes (peaked T waves, flattened P waves, prolonged PR interval, widened QRS) indicates urgent treatment regardless of the absolute potassium level. 2

Immediate Management (Severe Hyperkalemia or ECG Changes)

Step 1: Cardiac Membrane Stabilization

Administer IV calcium immediately for any patient with severe hyperkalemia (K+ >6.0 mEq/L) or ECG changes, regardless of potassium level. 1

• Calcium gluconate (10%): 15-30 mL IV over 2-5 minutes 3, 2
• Calcium chloride (10%): 5-10 mL (500-1000 mg) IV over 2-5 minutes 3
• Effects begin within 1-3 minutes but last only 30-60 minutes 1, 2
• Critical caveat: Calcium does NOT lower serum potassium—it only stabilizes cardiac membranes temporarily 2

Step 2: Intracellular Potassium Shifting

Insulin with glucose is the most effective immediate treatment for rapidly lowering serum potassium. 3

• Standard regimen: 10 units regular insulin IV with 25g glucose (50 mL of D50W) over 15-30 minutes 3
• Onset of action: 15-30 minutes 1
• Duration of effect: 4-6 hours 1
• Monitor glucose closely to prevent hypoglycemia, especially in patients with low baseline glucose, no diabetes history, female sex, or renal dysfunction 2
• Can be repeated every 4-6 hours if hyperkalemia persists 2

Adjunctive therapies for potassium shifting:

• Nebulized albuterol: 20 mg in 4 mL nebulized 2

  • Augments insulin/glucose effects 1
  • Duration: 2-4 hours 2
  • Less effective as monotherapy 4

• Sodium bicarbonate: 50 mEq IV over 5 minutes 3

  • ONLY use in patients with concurrent metabolic acidosis (pH <7.35, bicarbonate <22 mEq/L) 1, 2
  • Onset: 30-60 minutes 2
  • Promotes potassium excretion through increased distal sodium delivery 1
  • Do NOT use in patients without acidosis—evidence of efficacy is poor 2, 5

Step 3: Total Body Potassium Elimination

Loop diuretics for patients with adequate renal function:

• Furosemide: 40-80 mg IV 1, 2
• Only effective if GFR ≥50 mL/min/1.73m² 1
• Increases urinary potassium excretion 1

Hemodialysis for severe cases:

• Most effective and reliable method for potassium removal 2
• Indicated for: severe hyperkalemia unresponsive to medical management, oliguria, or end-stage renal disease 2

Chronic/Recurrent Hyperkalemia Management

Medication Review and Adjustment

Identify and address contributing medications before discontinuing life-saving RAAS inhibitors. 1

Medications to eliminate or reduce: 2

• NSAIDs
• Trimethoprim
• Heparin 2
• Beta-blockers
• Potassium supplements
• Salt substitutes (contain potassium chloride)

RAAS Inhibitor Management Algorithm

For patients on RAAS inhibitors (ACE inhibitors, ARBs, mineralocorticoid antagonists): 1

• K+ 5.0-6.5 mEq/L: Initiate approved potassium-lowering agent while MAINTAINING RAAS inhibitor therapy 1, 2
• K+ >6.5 mEq/L: Temporarily discontinue or reduce RAAS inhibitor dose AND initiate potassium-lowering agent 1
• Once K+ controlled (<5.0 mEq/L): Reintroduce RAAS inhibitors at lower doses with close monitoring 1

Do NOT permanently discontinue RAAS inhibitors—these provide mortality benefit in cardiovascular and renal disease. 2

Newer Potassium Binders (Preferred for Long-Term Management)

Patiromer (Veltassa): 2

• Starting dose: 8.4 g once daily
• Titrate up to 25.2 g daily based on potassium levels
• Onset of action: ~7 hours
• Safer alternative to sodium polystyrene sulfonate 1

Sodium zirconium cyclosilicate (SZC/Lokelma): 2

• Acute phase: 10 g three times daily for 48 hours
• Maintenance: 5-15 g once daily
• Onset of action: ~1 hour (fastest-acting oral agent) 2
• Effective for both acute (K+ ≥5.8 mEq/L) and chronic management 2

Avoid chronic use of sodium polystyrene sulfonate (Kayexalate): 1, 2

• Risk of bowel necrosis, especially with sorbitol 1
• Delayed onset of action 2
• Not recommended for acute or chronic management 1

Diuretic Optimization

• Loop diuretics (furosemide 40-80 mg daily) or thiazide diuretics promote urinary potassium excretion 2
• Only effective with adequate renal function 1

Monitoring Protocol

Initial monitoring after acute treatment: 3

• Serial potassium levels at 1,2,4, and 6 hours after treatment initiation 3
• Continuous cardiac monitoring until potassium normalizes 3
• Monitor for rebound hyperkalemia 2-4 hours after insulin/glucose administration 3

Chronic monitoring for high-risk patients: 1, 2

• Check potassium within 1 week of starting or escalating RAAS inhibitors 2
• Reassess 7-10 days after initiating potassium binder therapy 2
• More frequent monitoring for patients with CKD, heart failure, diabetes, or history of hyperkalemia 2

Special Populations

Patients with Chronic Kidney Disease

• Optimal potassium range is broader in advanced CKD: 3.3-5.5 mEq/L for stage 4-5 CKD versus 3.5-5.0 mEq/L for stage 1-2 CKD 2
• Aggressively maintain RAAS inhibitors in proteinuric CKD using potassium binders—these drugs slow CKD progression 2
• Loop diuretics remain effective with GFR ≥50 mL/min/1.73m² 1

Patients with Advanced Liver Disease and Renal Impairment

• Insulin with glucose is the most appropriate immediate treatment 3
• Consider sodium bicarbonate if metabolic acidosis is present (common in liver disease) 3
• These patients are at particularly high risk for severe hyperkalemia and require careful management 3

Critical Pitfalls to Avoid

• Do NOT rely solely on ECG findings—they are highly variable and less sensitive than laboratory tests 2
• Do NOT use sodium bicarbonate without metabolic acidosis—it is only indicated when pH <7.35 2
• Do NOT forget glucose with insulin—hypoglycemia risk is significant 2
• Do NOT assume calcium, insulin, or beta-agonists remove potassium—they only temporize; definitive elimination strategies are required 2
• Do NOT delay treatment when K+ >5.0 mEq/L in high-risk patients (CKD, heart failure, on RAAS inhibitors) 1
• Do NOT discontinue beneficial RAAS inhibitor therapy prematurely—manage hyperkalemia with potassium binders instead 1, 2
• Do NOT use chronic sodium polystyrene sulfonate—bowel necrosis risk is unacceptable 1

Dietary Considerations

Evidence linking dietary potassium intake to serum potassium is limited. 2

• A potassium-rich diet provides cardiovascular benefits, including blood pressure reduction 2
• Dietary restriction should be nuanced, focusing on reducing nonplant sources of potassium rather than blanket restriction 6
• Avoid potassium supplements and salt substitutes in all hyperkalemic patients 2