Immediate Treatment for Hyperkalemia
For severe hyperkalemia (≥6.5 mEq/L) or any ECG changes, immediately administer intravenous calcium to stabilize cardiac membranes, followed simultaneously by insulin with glucose and nebulized albuterol to shift potassium intracellularly, then initiate definitive potassium removal strategies. 1
Severity Assessment
Before initiating treatment, rapidly classify the severity:
- Mild hyperkalemia: 5.0-5.9 mEq/L 1, 2
- Moderate hyperkalemia: 6.0-6.4 mEq/L 1, 2
- Severe hyperkalemia: ≥6.5 mEq/L (life-threatening) 1, 2
Critical point: ECG changes (peaked T waves, flattened P waves, prolonged PR interval, widened QRS) mandate urgent treatment regardless of the potassium level. 1, 2 Do not delay treatment waiting for repeat lab confirmation if ECG changes are present. 2
First, exclude pseudohyperkalemia from hemolysis, repeated fist clenching, or poor phlebotomy technique by repeating the measurement with appropriate technique or arterial sampling. 1, 2
Step 1: Cardiac Membrane Stabilization (Acts in 1-3 Minutes)
Administer intravenous calcium immediately if potassium >6.5 mEq/L OR any ECG changes are present. 1, 2
Calcium Options:
Key limitations: Calcium does NOT lower serum potassium—it only protects against arrhythmias temporarily for 30-60 minutes. 1, 2 Repeat dosing may be necessary if no ECG improvement within 5-10 minutes. 2 Monitor heart rate during administration and stop if symptomatic bradycardia occurs. 1
Step 2: Shift Potassium into Cells (Acts in 15-30 Minutes)
Administer all three agents together for maximum effect: 2
Insulin with Glucose (Primary Agent):
- 10 units regular insulin IV with 25g glucose (50 mL of D50W) over 15-30 minutes 1, 2
- Onset: 15-30 minutes; Duration: 4-6 hours 1, 2
- Critical: Always give glucose with insulin to prevent life-threatening hypoglycemia 2
- Can be repeated every 4-6 hours if hyperkalemia persists, with careful monitoring of glucose and potassium every 2-4 hours 2
- Patients at higher risk for hypoglycemia: low baseline glucose, no diabetes, female sex, altered renal function 2
Nebulized Beta-2 Agonist:
- Albuterol 10-20 mg nebulized over 15 minutes 1, 2
- Reduces serum potassium by approximately 0.5-1.0 mEq/L 1
- Onset: 15-30 minutes; Duration: 2-4 hours 1, 2
- Can augment insulin/glucose effects 3
Sodium Bicarbonate (ONLY if metabolic acidosis present):
- 50 mEq IV over 5 minutes 1, 2
- Only use if pH <7.35 and bicarbonate <22 mEq/L 1, 2
- Onset: 30-60 minutes 2
- Do not use without metabolic acidosis—it is ineffective and wastes time 2
Critical warning: These are temporizing measures only—they do NOT remove potassium from the body. 2 Rebound hyperkalemia can occur after 2 hours. 1
Step 3: Eliminate Potassium from Body (Definitive Treatment)
For Patients with Adequate Renal Function:
- Loop diuretics (furosemide 40-80 mg IV) to increase renal potassium excretion 1, 2
- Titrate to maintain euvolemia, not primarily for potassium management 2
For Chronic or Recurrent Hyperkalemia:
Newer potassium binders are preferred over traditional agents: 1, 2
Sodium zirconium cyclosilicate (SZC/Lokelma): 1, 2
- Acute: 10g three times daily for 48 hours
- Maintenance: 5-15g once daily
- Onset: ~1 hour (fastest option)
- Starting dose: 8.4g once daily with food
- Titrate up to 25.2g daily based on potassium levels
- Onset: ~7 hours
- Separate from other oral medications by at least 3 hours 2
Avoid sodium polystyrene sulfonate (Kayexalate): Associated with intestinal ischemia, colonic necrosis, and doubling of serious gastrointestinal adverse events. 1, 2
For Severe or Refractory Cases:
- Hemodialysis is the most effective and reliable method for severe hyperkalemia, especially in renal failure, oliguria, or cases unresponsive to medical management 1, 2, 4
Medication Management During Acute Episode
Immediately review and temporarily hold these medications: 2
- RAAS inhibitors (ACE inhibitors, ARBs, mineralocorticoid antagonists) if K+ >6.5 mEq/L 1, 2
- NSAIDs 1, 2
- Potassium-sparing diuretics (spironolactone, amiloride, triamterene) 2
- Trimethoprim 2
- Heparin 1, 2
- Beta-blockers 1, 2
- Potassium supplements and salt substitutes 1, 2
After Acute Resolution: Preventing Recurrence
For patients with cardiovascular disease or proteinuric CKD, do not permanently discontinue RAAS inhibitors—they provide mortality benefit and slow disease progression. 1, 2
Management Algorithm Based on Potassium Level:
K+ 4.5-5.0 mEq/L: Initiate/uptitrate RAAS inhibitor therapy with close monitoring 1
- Initiate potassium binder (patiromer or SZC)
- Maintain RAAS inhibitor therapy unless alternative treatable cause identified
- Monitor potassium closely
- Temporarily discontinue or reduce RAAS inhibitor
- Initiate potassium binder when levels >5.0 mEq/L
- Restart RAAS inhibitor at lower dose once K+ <5.0 mEq/L with concurrent potassium binder
Monitoring Protocol
- Check potassium within 1 week of starting or escalating RAAS inhibitors 1, 2
- Reassess 7-10 days after initiating potassium binder therapy 2
- For severe initial hyperkalemia (>6.5 mEq/L), monitor every 2-4 hours initially due to rebound risk 2
- Individualize frequency based on CKD stage, heart failure, diabetes, and history of hyperkalemia 2
Critical Pitfalls to Avoid
- Never delay treatment while waiting for repeat labs if ECG changes are present 2
- Never give insulin without glucose—hypoglycemia can be life-threatening 2
- Never use sodium bicarbonate without metabolic acidosis—it is ineffective 2
- Never rely solely on ECG findings—they are highly variable and less sensitive than laboratory tests 2
- Remember calcium, insulin, and beta-agonists are temporizing only—they do NOT remove potassium from the body 2
- Do not permanently discontinue RAAS inhibitors in cardiovascular disease—use potassium binders instead 1, 2
- Monitor for hypoglycemia after insulin administration, especially in high-risk patients 2
- Watch for rebound hyperkalemia within 4-6 hours after temporary measures 1, 2