Immediate Treatment for Hyperkalemia
For severe hyperkalemia (≥6.5 mEq/L) or any ECG changes, immediately administer IV calcium gluconate 15-30 mL (10%) over 2-5 minutes to stabilize the cardiac membrane, followed simultaneously by insulin 10 units IV with 25g dextrose and nebulized albuterol 10-20 mg to shift potassium intracellularly. 1
Step 1: Cardiac Membrane Stabilization (Immediate - Within 1-3 Minutes)
Administer calcium first if any of the following are present:
- Potassium ≥6.5 mEq/L 2, 1
- ECG changes: peaked T waves, flattened P waves, prolonged PR interval, widened QRS 2, 1
- Any cardiac arrhythmia 1
Calcium dosing:
- Calcium gluconate (10%): 15-30 mL IV over 2-5 minutes (preferred for peripheral access) 2, 1
- Calcium chloride (10%): 5-10 mL IV over 2-5 minutes (more potent, requires central line when possible) 2, 1
Critical caveats:
- Calcium does NOT lower potassium—it only protects against arrhythmias for 30-60 minutes 2, 1
- If no ECG improvement within 5-10 minutes, repeat the dose 2
- Monitor continuously during administration; stop if bradycardia develops 2
- Never give calcium through the same IV line as bicarbonate (causes precipitation) 2
Step 2: Shift Potassium Into Cells (Onset 15-30 Minutes, Duration 4-6 Hours)
Administer all three agents together for maximum effect:
Insulin + Glucose:
- 10 units regular insulin IV with 25g dextrose (50 mL D50W) over 15-30 minutes 2, 1
- Verify potassium is not below 3.3 mEq/L before giving insulin 2
- Monitor glucose closely to prevent hypoglycemia 2
- Can repeat every 4-6 hours if hyperkalemia persists 2
Beta-2 Agonist:
- Nebulized albuterol 10-20 mg in 4 mL over 15 minutes 2, 1
- Effects last 2-4 hours 2
- Use as adjunctive therapy with insulin 2
Sodium Bicarbonate (ONLY if metabolic acidosis present):
- 50 mEq IV over 5 minutes 2, 1
- Only use if pH <7.35 and bicarbonate <22 mEq/L 2
- Effects take 30-60 minutes to manifest 2
- Do NOT use without documented acidosis—it wastes time and is ineffective 2
Step 3: Eliminate Potassium From Body (Definitive Treatment)
Choose based on severity and renal function:
For severe hyperkalemia (≥6.5 mEq/L) or renal failure:
- Hemodialysis is the most effective and reliable method 2, 1
- Indicated for: severe hyperkalemia unresponsive to medical management, oliguria, end-stage renal disease 2
For moderate hyperkalemia (6.0-6.4 mEq/L) with adequate renal function:
For chronic management or subacute treatment:
Newer potassium binders (preferred):
Avoid sodium polystyrene sulfonate (Kayexalate): delayed onset, limited efficacy, risk of bowel necrosis 2
Step 4: Address Underlying Causes
Immediately review and hold/reduce these medications:
- RAAS inhibitors (ACE inhibitors, ARBs, MRAs) if K+ >6.5 mEq/L 4, 2
- NSAIDs 2
- Potassium-sparing diuretics 2
- Trimethoprim, heparin, beta-blockers 2
- Potassium supplements and salt substitutes 2
For K+ 5.0-6.5 mEq/L on RAAS inhibitors:
- Initiate potassium binder and maintain RAAS inhibitor therapy (do NOT discontinue) 4, 2
- These medications provide mortality benefit in cardiovascular and renal disease 4, 2
Monitoring Protocol
Acute phase:
- Recheck potassium within 1-2 hours after insulin/glucose or beta-agonist therapy 2
- Continue monitoring every 2-4 hours until stabilized 2
- Obtain ECG if initial presentation included cardiac changes to document resolution 2
After acute resolution:
- Check potassium within 7-10 days after starting or adjusting RAAS inhibitors 2
- Monitor more frequently in high-risk patients: CKD, diabetes, heart failure 2
Critical Pitfalls to Avoid
- Never delay calcium administration while waiting for repeat labs if ECG changes are present 2
- Never use sodium bicarbonate without documented metabolic acidosis 2
- Never give insulin without glucose—hypoglycemia can be life-threatening 2
- Remember: calcium, insulin, and beta-agonists are temporizing measures only—they do NOT remove potassium from the body 2
- Do not permanently discontinue RAAS inhibitors—use potassium binders to enable continuation of these life-saving medications 4, 2
- Exclude pseudohyperkalemia from hemolysis or improper sampling before initiating aggressive treatment 2