Management of Hyperkalemia: A Structured Approach
For hyperkalemia management, begin with membrane stabilization using IV calcium gluconate 10% (10-30 mL) for severe cases or those with ECG changes, followed by insulin with glucose and beta-agonists for redistribution, then implement appropriate potassium elimination strategies based on severity and clinical context. 1
Assessment of Severity
Hyperkalemia severity is classified based on potassium levels:
- Mild: K+ 5.5-6.0 mmol/L
- Moderate: K+ 6.1-6.5 mmol/L
- Severe: K+ >6.5 mmol/L 1
ECG changes to monitor:
- K+ 5.5-6.5 mmol/L: Peaked/tented T waves, ST-segment abnormalities
- K+ 6.5-7.5 mmol/L: PR interval prolongation, P wave flattening
- K+ 7.0-8.0 mmol/L: QRS widening, deepened S waves
- K+ >10 mmol/L: Sine wave pattern, ventricular fibrillation, asystole 1
Acute Hyperkalemia Management
Step 1: Membrane Stabilization (Immediate Action)
- Calcium gluconate 10%: 10-30 mL IV over 2-5 minutes
- Onset: 1-3 minutes
- Duration: 30-60 minutes
- Repeat after 5-10 minutes if ECG changes persist 1
Step 2: Intracellular Potassium Shift (15-30 minute onset)
Insulin with glucose: 10 units regular insulin IV with 50 mL of 25% dextrose
Nebulized beta-agonists: 10-20 mg salbutamol nebulized over 15 minutes
- Duration: 2-4 hours 1
Sodium bicarbonate: 50 mEq IV over 5 minutes (if metabolic acidosis present)
- Duration: 1-2 hours 1
Step 3: Potassium Elimination
Loop diuretics: 40-80 mg IV furosemide (for patients with adequate renal function)
- Onset: 30-60 minutes
- Duration: 2-4 hours 1
Potassium binders:
- Patiromer (Veltassa):
- Adults: Starting dose 8.4 g orally once daily
- Adjust by 8.4 g increments weekly to target potassium level
- Maximum dose: 25.2 g daily
- Pediatric patients (12-17 years): Starting dose 4 g once daily, adjust by 4 g increments
- Note: Not for emergency treatment due to delayed onset 3
- Patiromer (Veltassa):
Hemodialysis: For severe, refractory hyperkalemia, especially in patients with:
- Oliguric/anuric renal failure
- End-stage renal disease
- Persistent ECG changes despite treatment
- K+ >6.5 mEq/L resistant to medical therapy 1
Chronic Hyperkalemia Management
Identify and address underlying causes:
- Medication review (RAASi, NSAIDs, potassium-sparing diuretics)
- Renal function assessment
- Hormonal disorders (hypoaldosteronism)
Dietary modifications:
Medication management:
- Patiromer (Veltassa):
- Adults: 8.4 g once daily, titrate weekly by 8.4 g increments
- Maximum: 25.2 g daily
- Take other oral medications at least 3 hours before or after patiromer 3
- Patiromer (Veltassa):
Monitoring:
- Check serum potassium within 1 week of treatment initiation
- More frequent monitoring for patients with CKD, heart failure, or diabetes 1
Special Considerations
RAASi therapy: Consider continuing RAASi therapy when indicated, with close monitoring of potassium levels. Discontinuation of RAASi therapy is associated with higher risk of mortality and cardiovascular events 2
Drug interactions: Patiromer can bind to other oral medications. Administer other oral medications at least 3 hours before or after patiromer 3
Calcium administration caution: While calcium gluconate is effective for main rhythm disorders due to hyperkalemia, it may have limited effect on non-rhythm ECG disorders 4
Common Pitfalls to Avoid
Delayed recognition: Early recognition of moderate to severe hyperkalemia is vital in preventing fatal cardiac arrhythmias and muscle paralysis 5
Overreliance on sodium polystyrene sulfonate: Newer potassium binders like patiromer have improved safety profiles 1
Inadequate monitoring: Regular monitoring of serum potassium, especially after medication changes, is essential to prevent rebound hyperkalemia 1
Failure to address underlying causes: Identifying and treating the underlying cause of hyperkalemia is crucial for long-term management
Neglecting drug interactions: Patiromer can decrease absorption of certain medications when administered simultaneously 3
By following this structured approach to hyperkalemia management, clinicians can effectively address this potentially life-threatening electrolyte disorder while minimizing complications and optimizing patient outcomes.