Hyperkalemia Management
Immediate Assessment and Risk Stratification
For any patient with hyperkalemia, immediately obtain an ECG and classify severity based on potassium level and cardiac changes—this determines your treatment pathway. 1, 2
Severity Classification
- 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
- ECG changes mandate urgent treatment regardless of potassium level: peaked T waves, flattened P waves, prolonged PR interval, widened QRS 1, 2
Critical pitfall: Exclude pseudohyperkalemia from hemolysis, repeated fist clenching, or poor phlebotomy technique before initiating aggressive treatment—repeat the sample with proper technique or use arterial sampling if uncertain. 2
Severe Hyperkalemia (≥6.5 mEq/L or ECG Changes)
This is a medical emergency requiring immediate three-step treatment within minutes. 1, 3, 4
Step 1: Cardiac Membrane Stabilization (Immediate—Within 1-3 Minutes)
Administer IV calcium first to prevent fatal arrhythmias—this is your most urgent intervention. 1, 2, 3
- Calcium chloride 10%: 5-10 mL (500-1000 mg) IV over 2-5 minutes (preferred for rapid effect) 1, 3
- Alternative: Calcium gluconate 10%: 15-30 mL IV over 2-5 minutes (use for peripheral IV access) 1, 2
- Onset: 1-3 minutes; Duration: 30-60 minutes only 1, 2
- Monitor ECG continuously during administration 2
- If no ECG improvement within 5-10 minutes, repeat the dose 2
Critical understanding: Calcium does NOT lower potassium—it only temporarily stabilizes cardiac membranes against arrhythmias. 1, 2, 3
Administration warning: Use central venous access for calcium chloride when possible, as extravasation causes severe tissue injury; stop if symptomatic bradycardia occurs. 1
Step 2: Shift Potassium Into Cells (Onset 15-30 Minutes, Duration 4-6 Hours)
Administer all three agents simultaneously for maximum effect—these are temporizing measures only. 1, 2
Insulin 10 units regular IV + 25g glucose (50 mL D50W) over 15-30 minutes 1, 2, 3
Sodium bicarbonate 50 mEq IV over 5 minutes ONLY if metabolic acidosis present (pH <7.35, bicarbonate <22 mEq/L) 1, 2
Critical pitfall: These measures provide only transient effects (1-4 hours), and rebound hyperkalemia can occur after 2 hours—you MUST initiate definitive potassium removal simultaneously. 1
Step 3: Eliminate Potassium From Body (Definitive Treatment)
Choose based on renal function and clinical urgency. 1, 2, 3
Loop diuretics (furosemide 40-80 mg IV): Only effective with adequate renal function (eGFR >30 mL/min) 1, 2, 3
Hemodialysis: Most effective and reliable method for severe hyperkalemia, especially with renal failure, oliguria, or refractory cases 1, 2, 3
- Monitor for rebound hyperkalemia 4-6 hours post-dialysis 2
Newer potassium binders (for subacute management after stabilization):
Avoid sodium polystyrene sulfonate (Kayexalate): Delayed onset, risk of bowel necrosis, and should NOT be used for acute management. 1, 2, 5
Medication Management During Acute Episode
Temporarily discontinue or reduce these medications at K+ ≥6.5 mEq/L: 2
- RAAS inhibitors (ACE inhibitors, ARBs, mineralocorticoid antagonists)
- NSAIDs
- Potassium-sparing diuretics (spironolactone, amiloride, triamterene)
- Trimethoprim
- Heparin
- Beta-blockers
- Potassium supplements and salt substitutes
Moderate Hyperkalemia (6.0-6.4 mEq/L Without ECG Changes)
Initiate intracellular shift and definitive removal without cardiac stabilization. 1, 3
- Insulin 10 units + glucose 25g IV 1, 3
- Nebulized albuterol 10-20 mg 1, 3
- Loop diuretics or potassium binders 1, 3
- Calcium only if ECG changes develop 2
For patients on RAAS inhibitors with cardiovascular disease or CKD: Initiate potassium binder (patiromer or SZC) and maintain RAAS inhibitor therapy rather than discontinuing these life-saving medications. 1, 2
Mild Hyperkalemia (5.0-5.9 mEq/L)
Focus on chronic management and preventing progression—no acute interventions needed. 1, 3
Medication Review and Optimization
Do NOT permanently discontinue RAAS inhibitors in patients with heart failure, cardiovascular disease, or proteinuric CKD—these provide mortality benefit. 1, 2
Instead, implement this algorithm: 2
- Review and eliminate contributing medications: NSAIDs, trimethoprim, heparin, beta-blockers, potassium supplements, salt substitutes
- Optimize diuretic therapy (furosemide 40-80 mg daily) if adequate renal function
- Initiate potassium binder to enable RAAS inhibitor continuation
Potassium Binder Therapy for Chronic Management
For patients requiring RAAS inhibitors with K+ 5.0-6.5 mEq/L, initiate a newer potassium binder while maintaining RAAS therapy. 1, 2
Patiromer (Veltassa): Start 8.4g once daily with food, separate from other medications by 3 hours, titrate to 25.2g based on response 2
Sodium zirconium cyclosilicate (SZC/Lokelma): 10g three times daily for 48 hours, then 5-15g once daily 2
Monitoring Protocol
Check potassium within 1 week of starting or escalating RAAS inhibitors or potassium binders. 2
Reassess 7-10 days after dose changes, then individualize based on: 2
- CKD stage (more frequent monitoring for stage 4-5)
- Heart failure severity
- Diabetes presence
- History of hyperkalemia
Target potassium ranges: 2
- Stage 1-2 CKD: 3.5-5.0 mEq/L
- Stage 4-5 CKD: 3.3-5.5 mEq/L (broader tolerance due to compensatory mechanisms)
Dietary Considerations
Evidence linking dietary potassium intake to serum levels is limited—do NOT impose stringent dietary restrictions in patients on potassium binders. 2
Potassium-rich diets provide cardiovascular benefits including blood pressure reduction. 2
Focus dietary restriction on: 2
- Eliminating high-potassium salt substitutes
- Reducing non-plant sources of potassium
- Avoiding herbal supplements (alfalfa, dandelion, horsetail, nettle)
Special Populations
Patients on RAAS Inhibitors with Cardiovascular Disease
Maintaining RAAS inhibitors using potassium binders is preferable to discontinuing therapy—these medications provide mortality benefit and prevent rebound hyperkalemia. 1, 2
Algorithm for K+ 5.0-6.5 mEq/L: 1, 2
- Initiate patiromer or SZC
- Maintain RAAS inhibitor at current dose
- Monitor potassium weekly until stable
Algorithm for K+ >6.5 mEq/L: 1, 2
- Temporarily discontinue or reduce RAAS inhibitor
- Initiate acute treatment (calcium, insulin, albuterol)
- Start potassium binder when K+ <5.5 mEq/L
- Restart RAAS inhibitor at lower dose once K+ <5.0 mEq/L
Patients with CKD
Maintain RAAS inhibitors aggressively in proteinuric CKD using potassium binders—these drugs slow CKD progression. 2
For CKD with adequate renal function (eGFR >30): Loop diuretics (furosemide 40-80 mg daily) to increase urinary potassium excretion 2
For advanced CKD (stage 4-5): Broader optimal potassium range (3.3-5.5 mEq/L) due to compensatory mechanisms, but target 4.0-5.0 mEq/L to minimize mortality risk 2
Hemodialysis Patients
Target predialysis potassium 4.0-5.5 mEq/L to minimize mortality risk. 2
First-line agent: SZC 5g once daily on non-dialysis days, adjust weekly in 5g increments based on predialysis potassium 2
Second-line agent: Patiromer 8.4g once daily with food, titrate to 16.8-25.2g daily 2
Monitor for rebound hyperkalemia 4-6 hours post-dialysis, especially with initial K+ >6.5 mEq/L or ongoing potassium release (tumor lysis syndrome, rhabdomyolysis). 2
Critical Pitfalls to Avoid
- Do NOT rely solely on ECG findings—they are highly variable and less sensitive than laboratory tests 2
- Do NOT use sodium bicarbonate without metabolic acidosis—it is only indicated when pH <7.35 1, 2
- Do NOT give insulin without glucose—hypoglycemia can be life-threatening 2
- Do NOT delay calcium administration while waiting for repeat labs if ECG changes present 2
- Remember calcium, insulin, and beta-agonists do NOT remove potassium—they only temporize for 30 minutes to 6 hours 1, 2
- Do NOT permanently discontinue RAAS inhibitors in heart failure or proteinuric CKD—use potassium binders instead 1, 2
- Avoid sodium polystyrene sulfonate (Kayexalate) due to bowel necrosis risk and delayed onset 1, 2, 5