Management of Hyperkalemia
Immediate Assessment and Risk Stratification
Obtain a 12-lead ECG immediately in all patients with suspected hyperkalemia, as ECG changes indicate urgent cardiotoxicity requiring emergent treatment regardless of the absolute potassium value. 1, 2 The presence of peaked T waves, flattened P waves, prolonged PR interval, or widened QRS complex mandates immediate intervention to prevent progression to sine-wave pattern, ventricular fibrillation, or asystole. 1, 2
Critical Caveats About ECG Findings
- ECG changes are highly variable and less sensitive than laboratory tests—the absence of ECG abnormalities does NOT exclude dangerous hyperkalemia, particularly in patients with chronic kidney disease, diabetes, or heart failure who may tolerate higher potassium levels without ECG manifestations. 1, 2
- In one retrospective study of 494 patients, 38.5% with hyperkalemia had completely normal ECGs, and abnormal findings were present in only 59.9% of mild cases and 61.2% of severe cases. 3
- Never delay treatment while awaiting repeat potassium levels if ECG changes are present—ECG abnormalities indicate urgent need for membrane stabilization. 1, 2
Severity Classification
- Mild hyperkalemia: 5.0–5.9 mEq/L 1
- Moderate hyperkalemia: 6.0–6.4 mEq/L 1
- Severe hyperkalemia: ≥6.5 mEq/L 1
Rule out pseudohyperkalemia from hemolysis, repeated fist clenching during phlebotomy, or improper blood sampling by repeating the measurement with appropriate technique or arterial sampling. 1
Emergency Treatment Algorithm for Severe Hyperkalemia (K⁺ ≥6.5 mEq/L or ANY ECG Changes)
Step 1: Cardiac Membrane Stabilization (Onset 1–3 Minutes)
Administer IV calcium immediately to stabilize the cardiac membrane and prevent fatal arrhythmias. 1, 2, 4, 5, 6, 7
- Calcium gluconate 10%: 15–30 mL IV over 2–5 minutes (preferred for peripheral access) 1, 2
- Calcium chloride 10%: 5–10 mL IV over 2–5 minutes (more potent; use via central line when available) 1, 2
Key Points:
- Calcium does NOT lower serum potassium—it only temporarily protects the heart for 30–60 minutes. 1, 2
- Repeat the dose if no ECG improvement within 5–10 minutes. 1
- In patients with malignant hyperthermia and hyperkalemia, use calcium only in extremis as it may contribute to myoplasmic calcium overload. 1
Step 2: Intracellular Potassium Shift (Onset 15–30 Minutes, Duration 4–6 Hours)
Administer all three agents simultaneously for maximum additive effect: 1, 2, 7
Insulin + Glucose (Most Effective)
- 10 units regular insulin IV push + 25 g dextrose (50 mL D50W) 1, 2, 4, 6, 7
- Lowers potassium by 0.5–1.2 mEq/L within 30–60 minutes 1
- Always give glucose with insulin to prevent life-threatening hypoglycemia. 1, 2
- Monitor blood glucose closely after administration 2
- Can be repeated every 4–6 hours as needed, carefully monitoring potassium and glucose 1
Nebulized Albuterol (Adjunctive)
- 10–20 mg albuterol in 4 mL nebulized over 10–15 minutes 1, 2, 4, 6, 7
- Lowers potassium by 0.5–1.0 mEq/L within 30 minutes 1
- Duration 2–4 hours; can be repeated every 2 hours if needed 1
- Combining insulin/glucose with albuterol provides additive benefit 1, 2
Sodium Bicarbonate (ONLY with Metabolic Acidosis)
- 50 mEq IV over 5 minutes 1, 2, 4, 6, 7
- Use ONLY when metabolic acidosis is documented (pH <7.35, bicarbonate <22 mEq/L) 1, 2
- Onset 30–60 minutes 1
- Ineffective as monotherapy without acidosis—do not waste time using it in non-acidotic patients 1, 2, 7
Step 3: Definitive Potassium Removal (Within Hours)
Recognize that calcium, insulin, and beta-agonists are temporizing measures only—they do NOT remove potassium from the body. 1, 2
Loop Diuretics (If Adequate Renal Function)
- Furosemide 40–80 mg IV 1, 4, 6
- Effective only when eGFR >30 mL/min and urine output is adequate 1
- Increases renal potassium excretion by stimulating flow to renal collecting ducts 1
Hemodialysis (Most Reliable Method)
Hemodialysis is the gold standard for rapid potassium removal. 1, 4, 6, 7 Absolute indications include: 1
- Serum potassium >6.5 mEq/L unresponsive to medical therapy
- Oliguria or anuria
- End-stage renal disease
- Ongoing potassium release (tumor lysis syndrome, rhabdomyolysis)
- Severe renal impairment (eGFR <15 mL/min)
- Persistent ECG changes despite medical management
In hemodynamically unstable patients, continuous renal replacement therapy (CRRT) is preferred over intermittent hemodialysis to minimize rapid fluid shifts and reduce intradialytic hypotension risk. 1
Potassium Binders (Sub-Acute Management)
- Sodium zirconium cyclosilicate (SZC/Lokelma): 10 g three times daily for 48 hours, then 5–15 g once daily for maintenance; onset ~1 hour 1
- Patiromer (Veltassa): 8.4 g once daily with food, titrated up to 25.2 g daily; onset ~7 hours 1
- Avoid sodium polystyrene sulfonate (Kayexalate) due to delayed onset, limited efficacy, and risk of bowel necrosis and colonic ischemia 1, 6
Medication Management During Acute Episode
Hold Immediately When K⁺ >6.5 mEq/L:
- RAAS inhibitors (ACE inhibitors, ARBs, mineralocorticoid receptor antagonists) 1
- NSAIDs 1
- Potassium-sparing diuretics 1
- Trimethoprim-containing agents 1
- Heparin 1
- Beta-blockers 1
- Potassium supplements and salt substitutes 1
After Acute Resolution:
- Restart RAAS inhibitors at a lower dose once potassium <5.0 mEq/L 1
- Initiate a potassium binder (SZC or patiromer) to enable continuation of life-saving RAAS therapy, which provides mortality benefit in cardiovascular and renal disease 1
Monitoring Protocol
Acute Phase:
- Continuous cardiac monitoring throughout treatment 1, 2, 6
- Re-measure serum potassium 1–2 hours after insulin/glucose or beta-agonist therapy 1, 2
- Continue potassium checks every 2–4 hours until stable 1
- Obtain repeat ECG to confirm resolution of prior cardiac changes 1, 2
Post-Acute Phase:
- Check potassium within 1 week after initiating or escalating RAAS inhibitors 1
- Reassess 7–10 days after starting a potassium binder 1
- Individualize monitoring frequency based on eGFR, heart failure status, diabetes, or prior hyperkalemia episodes 1
Chronic Hyperkalemia Management
For patients on RAAS inhibitors with potassium 5.0–6.5 mEq/L, initiate an approved potassium-lowering agent (patiromer or SZC) and maintain RAAS inhibitor therapy unless an alternative treatable cause is identified. 1 This approach allows continuation of life-saving cardiovascular medications that slow CKD progression and improve mortality. 1
For patients with potassium >6.5 mEq/L, discontinue or reduce RAAS inhibitors temporarily and initiate a potassium-lowering agent when levels >5.0 mEq/L. 1
Additional Chronic Management Strategies:
- Eliminate contributing medications: NSAIDs, trimethoprim, heparin, beta-blockers, potassium supplements, salt substitutes 1
- Optimize diuretic therapy with loop or thiazide diuretics (if eGFR >30 mL/min) 1
- Implement dietary potassium restriction, avoiding processed foods and salt substitutes 1
- Consider fludrocortisone (increases potassium excretion but carries risks of fluid retention, hypertension, and vascular injury) 1
Critical Pitfalls to Avoid
- Do NOT delay calcium administration while awaiting repeat potassium levels when ECG changes are present. 1, 2
- Never give insulin without glucose—hypoglycemia can be fatal. 1, 2
- Do NOT use sodium bicarbonate without documented metabolic acidosis—it is ineffective and wastes time. 1, 2, 7
- Do NOT rely solely on ECG findings—they are highly variable and less sensitive than laboratory tests. 1, 3
- Do NOT permanently discontinue RAAS inhibitors—use potassium binders to maintain these life-saving medications. 1
- Remember that calcium, insulin, and beta-agonists are temporizing measures only—they do NOT remove potassium from the body. 1, 2
Special Populations
Patients with CKD:
- Maintain RAAS inhibitors aggressively using potassium binders, as these drugs slow CKD progression 1
- Optimal potassium range is broader in advanced CKD: 3.3–5.5 mEq/L for stage 4–5 CKD versus 3.5–5.0 mEq/L for stage 1–2 CKD 1