Evaluation and Emergency Treatment of Hyperkalemia
Immediate Assessment
Obtain a 12-lead ECG immediately upon presentation, as ECG changes indicate severe cardiotoxicity requiring urgent treatment regardless of the absolute potassium value. 1
Critical ECG Findings by Severity
- Peaked/tented T waves (earliest sign): typically appear at K+ >5.5 mEq/L 1
- Moderate changes: flattened P waves, prolonged PR interval, widened QRS, deepened S waves (K+ ~6.0-6.4 mEq/L) 1
- Severe changes: sine-wave pattern, idioventricular rhythms, ventricular fibrillation, or asystole (K+ ≥6.5-7.0 mEq/L) 1
Essential Laboratory Workup
- Complete metabolic panel (electrolytes, BUN, creatinine, glucose) 2
- Complete blood count 2
- Urinalysis 2
- Venous blood gas if metabolic acidosis suspected (pH <7.35, bicarbonate <22 mEq/L) 2
- Repeat potassium measurement to exclude pseudohyperkalemia from hemolysis, fist clenching, or poor phlebotomy technique 1
Important caveat: ECG findings are highly variable and less sensitive than laboratory testing—absence of ECG changes does NOT rule out dangerous hyperkalemia, particularly in patients with chronic kidney disease, diabetes, or heart failure who may tolerate higher levels without ECG manifestations. 3
Emergency Treatment Algorithm
STEP 1: Cardiac Membrane Stabilization (if K+ ≥6.5 mEq/L OR any ECG changes)
Administer IV calcium immediately—this is the ONLY immediate protection against fatal arrhythmias. 1, 2
- Calcium gluconate 10%: 15-30 mL IV over 2-5 minutes (preferred for peripheral access) 1
- OR calcium chloride 10%: 5-10 mL (500-1000 mg) IV over 2-5 minutes (if central access available) 1
- Onset: 1-3 minutes 1
- Duration: 30-60 minutes (temporary only) 1
- Repeat dose: If no ECG improvement within 5-10 minutes, give second dose 3
Critical pitfall: Calcium does NOT lower potassium—it only stabilizes cardiac membranes temporarily. Never delay calcium while waiting for repeat labs if ECG changes are present. 1, 2
STEP 2: Shift Potassium Intracellularly (Administer ALL Simultaneously)
Insulin-Glucose (First-Line)
- 10 units regular insulin IV + 25g dextrose (50 mL D50W) over 15-30 minutes 1
- Effect: Lowers K+ by 0.5-1.2 mEq/L within 30-60 minutes, lasts 4-6 hours 1
- Monitor glucose closely to prevent life-threatening hypoglycemia 3
- Never give insulin without glucose 2
Nebulized Albuterol (Adjunctive)
- 10-20 mg albuterol in 4 mL nebulized over 10-15 minutes 1
- Effect: Lowers K+ by 0.5-1.0 mEq/L within 30 minutes, lasts 2-4 hours 1
- Can repeat every 2 hours if needed 2
- Combining insulin/glucose with albuterol provides additive benefit 3
Sodium Bicarbonate (ONLY if Metabolic Acidosis Present)
- 50 mEq IV over 5 minutes 1
- Use ONLY when: pH <7.35 AND bicarbonate <22 mEq/L 1, 2
- Onset: 30-60 minutes (slower than insulin/beta-agonists) 2
- Poor efficacy when used alone 1
Critical pitfall: Never use sodium bicarbonate without documented metabolic acidosis—it is ineffective and wastes time. 2
STEP 3: Remove Potassium from Body (Definitive Treatment)
Loop Diuretics (if Adequate Renal Function)
- Furosemide 40-80 mg IV 1
- Effective only when: eGFR >30 mL/min and patient is non-oliguric 2
- Mechanism: Increases urinary potassium excretion 1
Hemodialysis (Most Reliable Method)
Hemodialysis is the gold standard for severe hyperkalemia and should be initiated urgently when: 2, 4
- K+ >6.5 mEq/L unresponsive to medical therapy 2
- Oliguria or anuria 2
- End-stage renal disease 2
- Ongoing potassium release (tumor lysis syndrome, rhabdomyolysis) 2
- eGFR <15 mL/min 2
- Persistent ECG changes despite medical management 2
For hemodynamically unstable patients: Continuous renal replacement therapy (CRRT) is preferred over intermittent hemodialysis to minimize rapid fluid shifts and intradialytic hypotension. 2
Potassium Binders (Sub-acute Management)
- Sodium zirconium cyclosilicate (SZC/Lokelma): 10g three times daily for 48 hours, then 5-15g once daily; onset ~1 hour 2
- Patiromer (Veltassa): 8.4g once daily with food, titrated up to 25.2g daily; onset ~7 hours 2
- Avoid sodium polystyrene sulfonate (Kayexalate): Risk of bowel necrosis, colonic ischemia, and limited efficacy data 2
STEP 4: Medication Management During Acute Episode
Immediately hold when K+ >6.5 mEq/L: 2
- RAAS inhibitors (ACE inhibitors, ARBs, mineralocorticoid receptor antagonists)
- NSAIDs
- Potassium-sparing diuretics (spironolactone, amiloride, triamterene)
- Trimethoprim-containing agents
- Heparin
- Beta-blockers
- Potassium supplements and salt substitutes
After acute resolution (K+ <5.0 mEq/L): 2
- Restart RAAS inhibitors at lower dose with concurrent potassium binder
- Do NOT permanently discontinue RAAS inhibitors—they provide mortality benefit in cardiovascular and renal disease 2
Monitoring Protocol
Acute Phase
- Recheck potassium 1-2 hours after insulin/glucose or beta-agonist therapy 2
- Continue checks every 2-4 hours until stable 2
- Repeat ECG to confirm resolution of cardiac changes 2
- Monitor blood glucose closely after insulin administration (risk higher in patients with low baseline glucose, no diabetes, female sex, or impaired renal function) 2
Post-Acute Phase
- Check potassium within 1 week after initiating or escalating RAAS inhibitors 1
- Reassess 7-10 days after starting potassium binder 1
- Individualize monitoring frequency based on eGFR, heart failure, diabetes, or history of hyperkalemia 2
Common Pitfalls to Avoid
- Never delay calcium administration while awaiting repeat potassium levels when ECG changes are present 2
- Never give insulin without glucose—hypoglycemia can be fatal 2
- Recognize that calcium, insulin, and beta-agonists are temporizing measures only—they do NOT remove potassium from the body 2
- Do not use sodium bicarbonate without documented metabolic acidosis 2
- Do not rely solely on ECG findings—they are highly variable and less sensitive than laboratory tests 1
- Do not permanently discontinue RAAS inhibitors—use potassium binders to maintain these life-saving medications 2