Management of Potassium Disorders
Hyperkalemia Management
Immediate Assessment and Classification
For hyperkalemia, immediately verify the result is not pseudohyperkalemia from hemolysis or poor phlebotomy technique by repeating the measurement, then classify severity and obtain an ECG to guide treatment urgency. 1, 2
- Severity classification: Mild (5.0-5.9 mEq/L), Moderate (6.0-6.4 mEq/L), Severe (≥6.5 mEq/L) 1, 2
- ECG changes indicating urgent treatment regardless of potassium level: peaked T waves, flattened P waves, prolonged PR interval, widened QRS complexes 1, 2
- Do not rely solely on ECG findings—they are highly variable and less sensitive than laboratory tests 1, 2
Acute Hyperkalemia Treatment Algorithm
For potassium ≥6.5 mEq/L or any ECG changes, immediately administer IV calcium gluconate to stabilize cardiac membranes, followed by insulin with glucose and nebulized albuterol to shift potassium intracellularly. 1, 2
Step 1: Cardiac Membrane Stabilization (Onset: 1-3 minutes, Duration: 30-60 minutes)
- Calcium gluconate 10%: 15-30 mL IV over 2-5 minutes (preferred) 3, 1, 2
- Alternative: Calcium chloride 10%: 5-10 mL IV over 2-5 minutes 1, 2
- Critical caveat: Calcium does NOT lower potassium—it only temporizes cardiac risk 1, 2
- In cardiac arrest, use calcium chloride instead of calcium gluconate 4
Step 2: Intracellular Potassium Shift (Onset: 15-30 minutes, Duration: 4-6 hours)
- Insulin 10 units IV with 50 mL of 50% dextrose (25g glucose) 3, 1, 2
- Alternative dosing: 0.1 units/kg (approximately 5-7 units in adults) 3
- Must verify potassium is not below 3.3 mEq/L before administering insulin 3
- Always administer glucose with insulin to prevent hypoglycemia 1, 2
- Monitor glucose and potassium every 2-4 hours after administration 3
- Can repeat insulin/glucose every 4-6 hours if hyperkalemia persists 3
Step 3: Adjunctive Intracellular Shift
- Nebulized albuterol 20 mg in 4 mL (effects last 2-4 hours) 3, 1, 2
- Beta-agonists augment insulin effects but do not remove potassium from the body 1, 5
Step 4: Sodium Bicarbonate (ONLY if metabolic acidosis present)
- Use ONLY when pH <7.35 and bicarbonate <22 mEq/L 3, 1
- Onset of action: 30-60 minutes 1
- Do not use in patients without metabolic acidosis—this is a common pitfall 1, 2
Step 5: Potassium Removal from Body
- Loop diuretics (furosemide 40-80 mg IV) if adequate kidney function present 1, 2
- Hemodialysis is the most effective and reliable method for severe hyperkalemia, especially with renal failure or cases unresponsive to medical management 3, 1, 6
Chronic Hyperkalemia Management
For chronic hyperkalemia, maintain life-saving RAAS inhibitors by using newer potassium binders (patiromer or sodium zirconium cyclosilicate) rather than discontinuing these medications. 1
Medication Review and Adjustment
- Eliminate or reduce contributing medications: NSAIDs, trimethoprim, heparin, beta-blockers, potassium supplements, salt substitutes 1
- Do NOT discontinue RAAS inhibitors (ACE inhibitors, ARBs, mineralocorticoid antagonists) as they provide mortality benefit 1
Potassium Binder Selection
For potassium 5.0-6.5 mEq/L on RAAS inhibitors: Initiate approved potassium-lowering agent and maintain RAAS therapy 3, 1
- Sodium zirconium cyclosilicate (SZC/Lokelma): 10g three times daily for 48 hours, then 5-15g once daily for maintenance (onset: ~1 hour) 1
- Patiromer (Veltassa): Starting at 8.4g once daily, titrated up to 25.2g daily based on potassium levels (onset: ~7 hours) 1
- These newer agents are preferred over sodium polystyrene sulfonate (Kayexalate), which has delayed onset and risk of bowel necrosis 1, 4
For potassium >6.5 mEq/L on RAAS inhibitors: Temporarily discontinue or reduce RAAS inhibitor, initiate potassium-lowering agent when levels >5.0 mEq/L 1
Diuretic Therapy
- Loop or thiazide diuretics promote urinary potassium excretion by increasing distal sodium delivery 3, 1, 2
- Fludrocortisone increases potassium excretion but carries risks of fluid retention, hypertension, and vascular injury 3, 1
Monitoring Protocol
- Check potassium within 1 week of starting or escalating RAAS inhibitors 1, 2
- Reassess 7-10 days after initiating potassium binder therapy 1, 2
- High-risk patients (CKD, heart failure, diabetes, history of hyperkalemia) require more frequent monitoring 1, 2
- For CKD stage 4-5, optimal potassium range is broader: 3.3-5.5 mEq/L versus 3.5-5.0 mEq/L for stage 1-2 1
Special Considerations for Mild Hyperkalemia (5.0-5.5 mEq/L)
- Do NOT initiate acute interventions (calcium, insulin, albuterol) for mild hyperkalemia without ECG changes or symptoms 1
- Consider loop diuretics to enhance urinary potassium excretion if adequate renal function 1
- Avoid potassium supplements and salt substitutes 1
- Dietary restriction should be approached cautiously—potassium-rich diets provide cardiovascular benefits including blood pressure reduction 1
Hypokalemia Management
Treatment Indications and Approach
Hypokalemia should be treated with oral or intravenous potassium, with the route and urgency determined by severity, symptoms, ECG changes, and comorbid conditions. 7, 8
Indications for Potassium Replacement
- Treatment of hypokalemia with or without metabolic alkalosis 7
- Digitalis intoxication 7
- Hypokalemic familial periodic paralysis 7
- Prevention of hypokalemia in high-risk patients (digitalized patients, significant cardiac arrhythmias) 7
Route Selection
- Oral potassium chloride is preferred for non-urgent cases and patients who can tolerate oral intake 7
- Intravenous potassium for severe or symptomatic hypokalemia, abrupt changes in potassium levels, ECG changes, or inability to take oral medications 8
- Extended-release preparations should be reserved for patients who cannot tolerate or refuse liquid/effervescent preparations or have compliance issues 7
Diuretic-Induced Hypokalemia
- Consider using a lower dose of diuretic rather than automatic supplementation 7
- Check serum potassium periodically 7
- Dietary supplementation with potassium-containing foods may be adequate for milder cases 7
- In more severe cases where diuretic dose adjustment is ineffective or unwarranted, supplementation with potassium salts is indicated 7
Key Pitfalls to Avoid
- Remember that calcium, insulin, and beta-agonists do NOT remove potassium from the body—they only temporize by shifting potassium intracellularly 1, 2
- Always ensure glucose is administered with insulin to prevent hypoglycemia 1, 2
- Do not use sodium bicarbonate without metabolic acidosis 1, 2
- Monitor for rebound potassium disturbances when treating transcellular shifts 8
- In digitalized patients, too rapid lowering of serum potassium can produce digitalis toxicity 7
- Extended-release potassium preparations can have delayed absorption and toxic effects for hours 7