Management of Hyperkalemia
Hyperkalemia management follows a three-tiered approach: immediate cardiac membrane stabilization with intravenous calcium, rapid intracellular potassium shift using insulin/glucose and beta-agonists, and definitive potassium removal through diuretics, potassium binders, or dialysis. 1
Classification and Initial Assessment
- Mild hyperkalemia: 5.0-5.9 mEq/L 2
- Moderate hyperkalemia: 6.0-6.4 mEq/L 2
- Severe hyperkalemia: ≥6.5 mEq/L 2
Critical pitfall: ECG changes (peaked T waves, flattened P waves, prolonged PR interval, widened QRS) indicate urgent treatment regardless of the absolute potassium level and mandate immediate therapy. 2 However, ECG findings are highly variable and less sensitive than laboratory tests—symptoms can be nonspecific, so do not rely solely on ECG to guide treatment urgency. 1
Acute Hyperkalemia Management
Step 1: Cardiac Membrane Stabilization (Onset: 1-3 minutes)
Administer calcium gluconate 10% solution: 15-30 mL IV over 2-5 minutes for any patient with severe hyperkalemia or ECG changes. 1, 2 Alternatively, calcium chloride 10%: 5-10 mL IV over 2-5 minutes can be used. 2
- Effects begin within 1-3 minutes but are temporary (30-60 minutes duration). 1, 2
- Does not lower serum potassium—only stabilizes cardiac membranes. 1
- If no ECG improvement within 5-10 minutes, repeat the dose. 1
- Exception: In malignant hyperthermia with hyperkalemia, use calcium only in extremis as it may worsen calcium overload. 2
Step 2: Intracellular Potassium Shift (Onset: 15-30 minutes)
Insulin with glucose is the primary shifting agent:
- Standard dose: 10 units regular insulin IV (some protocols use 0.1 units/kg or 5-7 units in adults). 2
- Administer with 25-50 grams of dextrose (typically D50W 50 mL) unless glucose >250 mg/dL. 1, 2
- Onset: 15-30 minutes; duration: 4-6 hours. 1, 2
- Critical safety measure: Verify potassium is not below 3.3 mEq/L before giving insulin. 2
- Monitor glucose every 1-2 hours and potassium every 2-4 hours after administration. 2
- High-risk patients for hypoglycemia: Low baseline glucose, no diabetes, female sex, altered renal function. 2
Beta-agonists (albuterol) augment insulin effects:
- Nebulized albuterol 10-20 mg can be administered. 3, 4
- Acts within 30 minutes to promote intracellular shift. 1
- Use in combination with insulin/glucose for additive effect. 4
Sodium bicarbonate has limited utility:
- Only use in patients with concurrent metabolic acidosis (pH <7.35, bicarbonate <22 mEq/L). 1, 2
- Promotes potassium excretion through increased distal sodium delivery and counters acidosis-induced potassium release. 1, 2
- Effects take 30-60 minutes—not immediate. 2
- Do not use routinely in non-acidotic patients. 1
Step 3: Definitive Potassium Removal
Loop diuretics (furosemide 40-80 mg IV):
- Increase renal potassium excretion in patients with adequate kidney function. 2
- Stimulate flow and delivery of potassium to renal collecting ducts. 1
- Limitation: Effectiveness depends on residual kidney function and may worsen renal function with volume depletion. 1
Hemodialysis:
- Most effective method for severe hyperkalemia, especially with renal failure or refractory cases. 1, 2, 5
- Use as adjunctive therapy after instituting other approaches. 1
- Essential for patients unresponsive to medical management. 5
Chronic Hyperkalemia Management
Medication Review and Adjustment
Identify and modify contributing medications:
- ACE inhibitors, ARBs, mineralocorticoid antagonists, NSAIDs, beta-blockers. 2
- For potassium 5.0-6.5 mEq/L on RAAS inhibitors: Initiate potassium-lowering agent and maintain RAAS inhibitor therapy unless alternative cause identified. 2
- For potassium >6.5 mEq/L: Temporarily discontinue or reduce RAAS inhibitors, initiate potassium-lowering agent, monitor closely. 2
Diuretic Therapy
Loop or thiazide diuretics promote urinary potassium excretion:
- First-line agents for chronic management. 1, 3, 2
- Risks: Gout, volume depletion, worsening kidney function, reduced effectiveness with declining renal function. 1
Fludrocortisone increases potassium excretion but carries significant risks:
Potassium Binders
Newer FDA-approved agents are preferred for long-term management:
Patiromer (Veltassa):
- FDA-approved for chronic hyperkalemia treatment. 1, 2
- Nonabsorbed cation exchanger that binds potassium in the GI tract. 1
Sodium zirconium cyclosilicate (Lokelma):
- FDA-approved for chronic hyperkalemia treatment. 1, 2, 6
- Limitation: Not for emergency treatment due to delayed onset of action. 6
Sodium polystyrene sulfonate (Kayexalate):
- Older agent with limited efficacy. 7
- Avoid chronic use, especially with sorbitol, due to risk of intestinal necrosis and severe GI complications. 8, 7
- Not indicated for emergency treatment due to delayed onset. 9
Special Populations and Monitoring
High-risk patients requiring frequent monitoring:
- Chronic kidney disease, heart failure, diabetes, cardiovascular disease on RAAS inhibitors. 2, 8
- Assess potassium 7-10 days after starting or increasing RAAS inhibitor doses. 2
Team-based approach is optimal:
- Involve cardiologists, nephrologists, primary care physicians, nurses, pharmacists, dietitians. 1, 3, 2
Dietary modification:
- Low-potassium diet counseling and adherence monitoring. 10
- Adequate hydration supports renal potassium excretion. 3
Clinical Algorithm Summary
- Severe hyperkalemia (≥6.5 mEq/L) or ECG changes: Calcium gluconate → Insulin/glucose + albuterol → Consider dialysis if refractory 1, 2
- Moderate hyperkalemia (6.0-6.4 mEq/L): Insulin/glucose + albuterol → Loop diuretics if adequate renal function → Potassium binders 2
- Mild hyperkalemia (5.0-5.9 mEq/L): Review medications → Diuretics → Potassium binders (patiromer or sodium zirconium cyclosilicate) 2
- Metabolic acidosis present: Add sodium bicarbonate to shifting regimen 1, 2
- Recurrent episodes: Initiate chronic potassium binder, optimize diuretics, maintain RAAS inhibitors when possible 2