Hyperkalemia Treatment
For acute hyperkalemia, immediately stabilize the cardiac membrane with intravenous calcium, shift potassium into cells with insulin/glucose and albuterol, then eliminate potassium from the body using diuretics, newer potassium binders, or hemodialysis—never use sodium polystyrene sulfonate for acute management due to delayed onset and serious safety concerns. 1, 2
Severity Assessment
Classify hyperkalemia severity to guide treatment urgency:
- Mild hyperkalemia: 5.0-5.9 mEq/L 1
- Moderate hyperkalemia: 6.0-6.4 mEq/L 1
- Severe hyperkalemia: ≥6.5 mEq/L, which is life-threatening 1
- ECG changes indicate urgent treatment regardless of potassium level, including peaked T waves, flattened P waves, prolonged PR interval, and widened QRS 1
Step 1: Cardiac Membrane Stabilization (Immediate Effect: 1-3 Minutes)
Administer intravenous calcium first if potassium >6.5 mEq/L OR any ECG changes are present:
- Calcium chloride (10%): 5-10 mL (500-1000 mg) IV over 2-5 minutes 1, 2
- Calcium gluconate (10%): 15-30 mL IV over 2-5 minutes as alternative 1, 2
- Calcium chloride is preferred as it provides more rapid increase in ionized calcium concentration than calcium gluconate, making it more effective in critically ill patients 1
- Effects begin within 1-3 minutes but last only 30-60 minutes 1, 2
- Calcium does NOT lower serum potassium—it only temporarily stabilizes cardiac membranes against arrhythmias 1, 2
- Repeat dose if no ECG improvement within 5-10 minutes: give second dose of 15-30 mL calcium gluconate IV over 2-5 minutes 2
- Administer through central line when possible, as extravasation through peripheral IV may cause severe tissue injury 1
- Monitor heart rate continuously and stop if symptomatic bradycardia occurs 1
Step 2: Shift Potassium Into Cells (Effect: 15-30 Minutes, Duration: 4-6 Hours)
Administer all three agents together for maximum effect:
Insulin with glucose: 10 units regular insulin IV with 25g glucose (50 mL of D50W) over 15-30 minutes 1, 2
- Onset within 15-30 minutes, effects last 4-6 hours 1
- Monitor for hypoglycemia, especially in patients with low baseline glucose, no diabetes, female sex, or altered renal function 1
- Verify potassium is not below 3.3 mEq/L before administering insulin 1
- Can be repeated every 4-6 hours if hyperkalemia persists, with careful glucose and potassium monitoring 1
Sodium bicarbonate: 50 mEq IV over 5 minutes ONLY if metabolic acidosis present (pH <7.35, bicarbonate <22 mEq/L) 1, 2
Critical caveat: These are temporizing measures only—rebound hyperkalemia can occur after 2 hours, so potassium-lowering agents must be initiated early 1
Step 3: Eliminate Potassium From Body (Definitive Treatment)
Choose method based on renal function and clinical urgency:
For Patients with Adequate Renal Function:
For All Patients (Preferred Long-Term Management):
Newer potassium binders are superior to sodium polystyrene sulfonate:
Sodium zirconium cyclosilicate (SZC/Lokelma):
Patiromer (Veltassa):
- Onset of action: ~7 hours 1, 2
- Starting dose: 8.4g once daily with food 1, 2
- Titrate up to 25.2g daily based on potassium levels 1, 2
- Separate from other oral medications by at least 3 hours 2
- Binds potassium in exchange for calcium in colon 2
- Monitor magnesium levels as patiromer causes hypomagnesemia 2
Avoid Sodium Polystyrene Sulfonate (Kayexalate):
- Should NOT be used for acute management due to delayed onset, limited efficacy, and risk of bowel necrosis 1, 2, 3
- FDA label states it "should not be used as an emergency treatment for life-threatening hyperkalemia because of its delayed onset of action" 3
- Associated with intestinal necrosis, colonic necrosis, and doubling of risk for serious gastrointestinal adverse events 2
- Concomitant use with sorbitol increases risk of intestinal necrosis 3
For Severe or Refractory Cases:
- Hemodialysis is the most effective and reliable method for severe hyperkalemia, especially in patients with renal failure 1, 2
- Reserved for severe cases unresponsive to medical management, oliguria, or end-stage renal disease 2
- Potassium levels can rebound 4-6 hours post-dialysis as intracellular potassium redistributes 2
Chronic Hyperkalemia Management
For patients on RAAS inhibitors with cardiovascular disease, maintaining these life-saving medications using potassium binders is preferable to discontinuing therapy:
- Potassium 5.0-6.5 mEq/L: Initiate patiromer or SZC while maintaining RAAS inhibitor therapy unless alternative treatable cause identified 1, 2
- Potassium >6.5 mEq/L: Temporarily discontinue or reduce RAAS inhibitor, initiate potassium-lowering agent when levels >5.0 mEq/L, monitor closely 1, 2
- Do NOT permanently discontinue RAAS inhibitors in patients with heart failure or proteinuric CKD, as these provide mortality benefit and slow disease progression 2
Review and adjust contributing medications:
- ACE inhibitors, ARBs, mineralocorticoid receptor antagonists 1, 2
- NSAIDs, trimethoprim, heparin, beta-blockers 1, 2
- Potassium supplements and salt substitutes 1, 2
- Avoid triple combination of ACE inhibitor + ARB + MRA due to excessive hyperkalemia risk 2
Monitoring Protocol
- Check potassium within 1 week of starting or escalating RAAS inhibitors 2
- Reassess 7-10 days after initiating potassium binder therapy 2
- Monitor every 2-4 hours during acute treatment until stabilized 2
- Individualize frequency based on CKD stage, heart failure, diabetes, and history of hyperkalemia 2
- Target potassium range: 4.0-5.0 mEq/L to minimize mortality risk 2
Critical Pitfalls to Avoid
- Never delay calcium administration while waiting for repeat labs if ECG changes present—ECG changes indicate urgent need regardless of exact potassium value 2
- Never use sodium bicarbonate without metabolic acidosis—it is ineffective without acidosis 1, 2
- Never give insulin without glucose—hypoglycemia can be life-threatening 2
- Never rely solely on ECG findings—they are highly variable and less sensitive than laboratory tests 2
- Remember calcium, insulin, and beta-agonists do NOT remove potassium—they only temporize, requiring concurrent initiation of elimination strategies 1, 2
- Do NOT use sodium polystyrene sulfonate for acute hyperkalemia due to delayed onset and serious safety concerns 1, 2, 3