Hyperkalemia Treatment Protocol
For severe hyperkalemia (≥6.5 mEq/L) or any ECG changes, immediately administer IV calcium gluconate 15-30 mL over 2-5 minutes to stabilize the cardiac membrane, followed simultaneously by insulin 10 units with 25g dextrose and nebulized albuterol 10-20 mg to shift potassium intracellularly, then initiate definitive potassium removal with loop diuretics or hemodialysis depending on renal function. 1
Classification and Urgency Assessment
Severity Categories:
ECG changes mandate immediate treatment regardless of potassium level 1, 3. Look specifically for peaked T waves, flattened P waves, prolonged PR interval, and widened QRS complex 1. However, ECG findings are highly variable and less sensitive than laboratory values—do not rely solely on ECG 1. Only 14% of hyperkalemic patients show ECG changes 4.
Exclude pseudohyperkalemia from hemolysis, repeated fist clenching, or poor phlebotomy technique before initiating aggressive treatment 1.
Step 1: Cardiac Membrane Stabilization (Onset 1-3 Minutes)
Administer IV calcium immediately if:
Dosing:
- Calcium gluconate 10%: 15-30 mL IV over 2-5 minutes (preferred for peripheral access) 1, 3
- Calcium chloride 10%: 5-10 mL IV over 2-5 minutes (more potent, requires central access) 1, 3
Critical points:
- Effect begins within 1-3 minutes but lasts only 30-60 minutes 1, 3
- Calcium does NOT lower potassium—it only protects the heart temporarily 1, 3
- Repeat dose if no ECG improvement within 5-10 minutes 1
- Monitor continuously during administration 1
- Never delay calcium while waiting for repeat labs if ECG changes are present 1
Step 2: Shift Potassium Intracellularly (Onset 15-30 Minutes)
Administer all three agents together for maximum effect 1:
Insulin-Glucose (Most Effective)
- 10 units regular insulin IV push + 25g dextrose (50 mL D50W) 1, 2, 3
- Onset: 15-30 minutes; duration: 4-6 hours 1, 3
- Reduces potassium by 0.5-1.2 mEq/L 1
- Never give insulin without glucose—hypoglycemia can be fatal 1
- Monitor glucose closely; risk higher in non-diabetics, females, low baseline glucose, and renal impairment 1
Nebulized Beta-Agonist
- Albuterol 10-20 mg in 4 mL nebulized over 10-15 minutes 1, 2, 3
- Onset: 30 minutes; duration: 2-4 hours 1, 3
- Reduces potassium by 0.5-1.0 mEq/L 1
- Can repeat every 2 hours if needed 1
- Augments insulin-glucose effect 1
Sodium Bicarbonate (ONLY with Metabolic Acidosis)
- 50 mEq IV over 5 minutes 1, 2, 3
- Use ONLY if pH <7.35 AND bicarbonate <22 mEq/L 1, 3
- Onset: 30-60 minutes 1, 3
- Ineffective without acidosis—do not waste time 1
Warning: These are temporizing measures only—rebound hyperkalemia occurs within 2-6 hours 1, 3. Definitive potassium removal must be initiated simultaneously 1.
Step 3: Definitive Potassium Removal
Loop Diuretics (First-Line if Adequate Renal Function)
- Furosemide 40-80 mg IV 1, 2, 3
- Effective only if eGFR >30 mL/min and non-oliguric 1
- Increases renal potassium excretion 1, 2
Hemodialysis (Most Effective Method)
Absolute indications: 1
- Potassium >6.5 mEq/L unresponsive to medical therapy
- Oliguria or anuria
- End-stage renal disease
- Ongoing potassium release (tumor lysis, rhabdomyolysis)
- eGFR <15 mL/min
- Persistent ECG changes despite treatment
Use continuous renal replacement therapy (CRRT) instead of intermittent hemodialysis in hemodynamically unstable patients 1.
Potassium Binders (Sub-Acute Management)
Newer agents (preferred):
- Sodium zirconium cyclosilicate (SZC/Lokelma): 10g three times daily for 48 hours, then 5-15g once daily 1
- Onset: ~1 hour (suitable for urgent scenarios) 1
- Patiromer (Veltassa): 8.4g once daily with food, titrated to 25.2g daily 1
Avoid sodium polystyrene sulfonate (Kayexalate): Associated with bowel necrosis, colonic ischemia, and lack of efficacy data 1, 5. The FDA label states it should NOT be used as emergency treatment due to delayed onset 5.
Medication Management During Acute Episode
Temporarily hold when potassium >6.5 mEq/L: 1
- RAAS inhibitors (ACE inhibitors, ARBs, mineralocorticoid antagonists)
- NSAIDs
- Potassium-sparing diuretics
- Trimethoprim
- Heparin
- Beta-blockers
- Potassium supplements and salt substitutes
After acute resolution: 1
- Restart RAAS inhibitors at lower dose once potassium <5.0 mEq/L
- Initiate potassium binder (SZC or patiromer) to enable continuation of life-saving RAAS therapy
- Never permanently discontinue RAAS inhibitors in cardiovascular disease or proteinuric CKD—they provide mortality benefit 1
Monitoring Protocol
Acute phase: 1
- Recheck potassium 1-2 hours after insulin/glucose or beta-agonist
- Continue checks every 2-4 hours until stable
- Repeat ECG to confirm resolution of changes
Post-acute phase: 1
- Check potassium within 1 week of starting/escalating RAAS inhibitors
- Reassess 7-10 days after initiating potassium binder
- Individualize frequency based on eGFR, heart failure, diabetes, or prior hyperkalemia
Critical Pitfalls to Avoid
- Do not delay calcium if ECG changes are present while awaiting repeat labs 1
- Never give insulin without glucose 1
- Do not use sodium bicarbonate without documented metabolic acidosis 1
- Remember calcium, insulin, and beta-agonists do NOT remove potassium—they only temporize 1
- Do not permanently discontinue RAAS inhibitors—use potassium binders instead 1
- Avoid sodium polystyrene sulfonate due to serious GI complications 1, 5
Special Populations
CKD patients: 1
- Maintain RAAS inhibitors aggressively using potassium binders—these drugs slow CKD progression
- Broader optimal potassium range: 3.3-5.5 mEq/L for stage 4-5 CKD
- Dialysis often required for definitive management in ESRD
Heart failure patients: 1
- Do not discontinue RAAS inhibitors or mineralocorticoid antagonists
- Use potassium binders to enable optimal medical therapy
- These medications provide mortality benefit