Management of Hyperkalemia
For acute hyperkalemia with ECG changes or potassium ≥6.5 mEq/L, immediately administer IV calcium gluconate 15-30 mL of 10% solution over 2-5 minutes to stabilize cardiac membranes, followed simultaneously by insulin 10 units with 25-50g dextrose IV and nebulized albuterol 20 mg to shift potassium intracellularly. 1
Initial Assessment and Classification
Before initiating treatment, verify the result is not pseudohyperkalemia from hemolysis, repeated fist clenching, or poor phlebotomy technique by repeating the measurement with proper technique or arterial sampling. 1, 2
Severity classification:
Obtain an ECG immediately to look for peaked T waves, flattened P waves, prolonged PR interval, and widened QRS complexes—these findings indicate urgent treatment regardless of the exact potassium level. 1 However, do not rely solely on ECG findings as they are highly variable and less sensitive than laboratory tests. 1
Acute Management Algorithm
Step 1: Cardiac Membrane Stabilization (Onset: 1-3 minutes, Duration: 30-60 minutes)
Administer IV calcium immediately if potassium >6.5 mEq/L OR any ECG changes are present. 1, 2
Dosing options:
- 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 1
Monitor ECG continuously during and for 5-10 minutes after administration. 1 If no ECG improvement within 5-10 minutes, repeat the dose. 1 Critical caveat: Calcium does NOT lower serum potassium—it only temporarily stabilizes cardiac membranes for 30-60 minutes. 1, 4
Step 2: Intracellular Potassium Shift (Onset: 15-30 minutes, Duration: 4-6 hours)
Give all three agents together for maximum effect: 1
Insulin + Glucose: 10 units regular insulin IV with 25-50g dextrose (50 mL of 50% dextrose or equivalent) 1, 2, 3
Nebulized Albuterol: 10-20 mg in 4 mL nebulized over 10 minutes 1, 3
Sodium Bicarbonate: 50 mEq IV over 5 minutes ONLY if metabolic acidosis is present (pH <7.35, bicarbonate <22 mEq/L) 1, 2
Step 3: Potassium Removal from the Body
Choose based on renal function and clinical context:
For patients with adequate kidney function:
- Loop diuretics (furosemide 40-80 mg IV) to increase renal potassium excretion 1, 4
- Titrate to maintain euvolemia, not primarily for potassium management 1
For severe hyperkalemia unresponsive to medical management, oliguria, or end-stage renal disease:
- Hemodialysis is the most effective and reliable method for potassium removal 1, 3, 4
- Can remove 25-50 mEq of potassium per hour 1
- Monitor for rebound hyperkalemia within 4-6 hours post-dialysis as intracellular potassium redistributes 1
Chronic Hyperkalemia Management
Medication Review and Adjustment
Immediately review and hold or reduce these medications: 1
- ACE inhibitors, ARBs, mineralocorticoid antagonists (MRAs) if K+ >6.0 mEq/L 1
- NSAIDs (attenuate diuretic effects and impair renal potassium excretion) 1
- Potassium-sparing diuretics (spironolactone, amiloride, triamterene) 1
- Trimethoprim, heparin, beta-blockers 1
- Potassium supplements and salt substitutes 1
Critical principle: The triple combination of ACE inhibitor + ARB + MRA is NOT recommended due to excessive hyperkalemia risk. 1
Potassium Binder Therapy
For patients requiring RAAS inhibitor continuation (cardiovascular disease, proteinuric CKD, heart failure):
First-line: Sodium Zirconium Cyclosilicate (SZC/Lokelma) 1, 5
- Dosing: 10g three times daily for 48 hours, then 5-15g once daily for maintenance 1
- Onset: ~1 hour (suitable for more urgent scenarios) 1
- Mechanism: Exchanges hydrogen and sodium for potassium 1
- Monitoring: Watch for edema due to sodium content 1
Second-line: Patiromer (Veltassa) 1, 5
- Dosing: Start 8.4g once daily with food, titrate up to 25.2g daily based on potassium levels 1
- Onset: ~7 hours 1
- Mechanism: Exchanges calcium for potassium in the colon 1
- Administration: Separate from other oral medications by at least 3 hours 1
- Monitoring: Check magnesium levels (causes hypomagnesemia) 1
Avoid: Sodium Polystyrene Sulfonate (Kayexalate) 1, 3
- Associated with intestinal ischemia, colonic necrosis, and doubling of risk for serious gastrointestinal adverse events 1
- Delayed onset of action and variable efficacy 1
RAAS Inhibitor Management Strategy
For patients with cardiovascular disease or proteinuric CKD, do NOT permanently discontinue RAAS inhibitors—they provide mortality benefit and slow disease progression. 1
Algorithm for RAAS inhibitor management: 1
- K+ 5.0-6.5 mEq/L: Initiate potassium binder (patiromer or SZC) and maintain RAAS inhibitor therapy 1
- K+ >6.5 mEq/L: Temporarily discontinue or reduce RAAS inhibitor, initiate potassium binder, monitor closely 1
- Once K+ <5.0 mEq/L: Restart RAAS inhibitor at lower dose with concurrent potassium binder therapy 1
Monitoring Protocol
Initial monitoring after starting or escalating RAAS inhibitors:
- Check potassium within 1 week of starting or dose escalation 1, 2
- Reassess 7-10 days after initiating potassium binder therapy 1
High-risk patients requiring more frequent monitoring: 1
- Chronic kidney disease (especially stage 4-5)
- Heart failure
- Diabetes mellitus
- History of hyperkalemia
- Multiple contributing medications
Target potassium ranges: 1
- Stage 1-2 CKD: 3.5-5.0 mEq/L
- Stage 4-5 CKD: 3.3-5.5 mEq/L (broader range due to compensatory mechanisms)
- Optimal range to minimize mortality: 4.0-5.0 mEq/L
Special Population: Hemodialysis Patients
For recurrent hyperkalemia in dialysis patients:
First-line: SZC 5g once daily on non-dialysis days, adjust weekly in 5g increments based on predialysis potassium 1
Second-line: Patiromer 8.4g once daily with food, titrate to 16.8-25.2g daily 1
Target predialysis potassium: 4.0-5.5 mEq/L to minimize mortality risk 1
Consider adjusting dialysate potassium concentration (typically 2.0-3.0 mEq/L) based on predialysis levels, but monitor for intradialytic arrhythmias with lower concentrations. 1
Critical Pitfalls to Avoid
Never delay treatment while waiting for repeat lab confirmation if ECG changes are present—ECG changes indicate urgent need regardless of the exact potassium value 1
Never give insulin without glucose—hypoglycemia can be life-threatening 1, 2
Never use sodium bicarbonate without metabolic acidosis—it is ineffective and wastes time 1, 2
Remember that calcium, insulin, and beta-agonists are temporizing measures only—they do NOT remove potassium from the body 1, 2, 4
Never administer calcium through the same IV line as sodium bicarbonate—precipitation will occur 1
Do not permanently discontinue RAAS inhibitors in patients with cardiovascular disease or proteinuric CKD—use potassium binders to enable continuation of these life-saving medications 1
Dietary Considerations
Evidence linking dietary potassium intake to serum potassium is limited, and a potassium-rich diet provides cardiovascular benefits including blood pressure reduction. 1 Newer potassium binders may allow for less restrictive dietary potassium restrictions, enabling patients to benefit from potassium-rich foods. 1 However, avoid potassium supplements and salt substitutes (which have high potassium content) in patients with hyperkalemia. 1