Management of Hyperkalemia
For acute severe hyperkalemia (≥6.5 mEq/L or any ECG changes), immediately administer IV calcium gluconate 15-30 mL of 10% solution over 2-5 minutes for cardiac membrane stabilization, followed simultaneously by insulin 10 units IV with 25g dextrose and nebulized albuterol 10-20 mg to shift potassium intracellularly, then initiate definitive potassium removal with loop diuretics or hemodialysis. 1
Initial Assessment and Classification
Verify true hyperkalemia by excluding pseudohyperkalemia from hemolysis, repeated fist clenching, or poor phlebotomy technique before initiating treatment. 1 Repeat the measurement with appropriate technique or arterial sampling if pseudohyperkalemia is suspected. 1
Classify severity as follows: 1
- Mild: 5.0-5.9 mEq/L
- Moderate: 6.0-6.4 mEq/L
- Severe: ≥6.5 mEq/L
Obtain an ECG immediately to assess for peaked T waves, flattened P waves, prolonged PR interval, or widened QRS complexes—these findings mandate urgent treatment regardless of the exact potassium level. 1 However, absent or atypical ECG changes do not exclude the necessity for immediate intervention. 2
Acute Hyperkalemia Management (K+ ≥6.5 mEq/L or ECG Changes)
Step 1: Cardiac Membrane Stabilization (Onset: 1-3 minutes)
Administer IV calcium first to protect against arrhythmias: 1
- Calcium gluconate 10%: 15-30 mL IV over 2-5 minutes (preferred for peripheral access) 1
- Calcium chloride 10%: 5-10 mL IV over 2-5 minutes (for central access or cardiac arrest) 1
Critical points about calcium: 1
- Effects begin within 1-3 minutes but last only 30-60 minutes 1
- Calcium does NOT lower potassium—it only stabilizes cardiac membranes temporarily 1
- Repeat dosing may be necessary if no ECG improvement within 5-10 minutes 1
- Continuous cardiac monitoring is mandatory during and after administration 1
- Never administer calcium through the same IV line as sodium bicarbonate (precipitation will occur) 1
Step 2: Shift Potassium Intracellularly (Onset: 15-30 minutes, Duration: 4-6 hours)
Administer all three agents together for maximum effect: 1
Insulin with glucose (first choice): 1
- Standard dose: 10 units regular insulin IV + 25g dextrose (50 mL of 50% solution) 1
- Alternative dose: 0.1 units/kg (approximately 5-7 units in adults) 1
- Critical: Never give insulin without glucose—hypoglycemia can be life-threatening 1
- Verify potassium is not below 3.3 mEq/L before administering insulin 1
- Monitor glucose every 2-4 hours after administration 1
- Patients at higher risk for hypoglycemia: low baseline glucose, no diabetes, female sex, altered renal function 1
Nebulized albuterol (adjunctive therapy): 1
Sodium bicarbonate (ONLY if metabolic acidosis present): 1
- Indication: pH <7.35, bicarbonate <22 mEq/L 1
- Dose: 50 mEq IV over 5 minutes 1
- Effects take 30-60 minutes to manifest 1
- Do not use without metabolic acidosis—it is ineffective and wastes time 1
Insulin can be repeated every 4-6 hours if hyperkalemia persists or recurs, with careful monitoring of potassium and glucose levels. 1
Step 3: Remove Potassium from the Body
Loop diuretics (if adequate renal function): 1
- Furosemide: 40-80 mg IV 1
- Increases renal potassium excretion by stimulating flow to renal collecting ducts 1
- Titrate to maintain euvolemia, not primarily for potassium management 1
Hemodialysis (most effective method): 1
- Reserved for severe cases unresponsive to medical management, oliguria, or end-stage renal disease 1
- Most reliable and effective method for potassium removal 1
- Monitor for rebound hyperkalemia within 4-6 hours post-dialysis as intracellular potassium redistributes 1
Step 4: Medication Review During Acute Episode
Temporarily discontinue or reduce at K+ ≥6.5 mEq/L: 1
- RAAS inhibitors (ACE inhibitors, ARBs, mineralocorticoid antagonists) 1
- NSAIDs 1
- Potassium-sparing diuretics (spironolactone, amiloride, triamterene) 1
- Trimethoprim 1
- Heparin 1
- Beta-blockers 1
- Potassium supplements and salt substitutes 1
Chronic Hyperkalemia Management (K+ 5.0-6.5 mEq/L)
Medication Optimization Strategy
For K+ 5.0-6.5 mEq/L: 1
- Maintain RAAS inhibitor therapy at current dose (provides mortality benefit in cardiovascular and renal disease) 1
- Initiate approved potassium-lowering agent (patiromer or sodium zirconium cyclosilicate) 1
- Eliminate contributing medications: NSAIDs, trimethoprim, heparin, potassium supplements, salt substitutes 1
For K+ >6.5 mEq/L: 1
- Temporarily reduce or hold RAAS inhibitor 1
- Initiate potassium-lowering agent 1
- Restart RAAS inhibitor at lower dose once potassium <5.0 mEq/L with concurrent potassium binder therapy 1
Never permanently discontinue RAAS inhibitors in patients with cardiovascular disease or proteinuric CKD—they provide mortality benefit and slow disease progression. 1
Potassium Binder Therapy (Preferred Agents)
Sodium zirconium cyclosilicate (SZC/Lokelma) - First choice for urgent scenarios: 1
- Acute phase: 10g three times daily for 48 hours 1
- Maintenance: 5-15g once daily 1
- Onset of action: ~1 hour 1
- Mechanism: Exchanges hydrogen and sodium for potassium 1
- Monitor for edema due to sodium content 1
Patiromer (Veltassa) - First choice for chronic management: 1
- Starting dose: 8.4g once daily with food 1
- Titration: Up to 25.2g daily based on potassium levels 1
- Onset of action: ~7 hours 1
- Mechanism: Exchanges calcium for potassium in the colon 1
- Separate from other oral medications by at least 3 hours 1
- Monitor magnesium levels (causes hypomagnesemia) 1
Sodium polystyrene sulfonate (Kayexalate) - AVOID: 3
- Should not be used as emergency treatment due to delayed onset of action 3
- Associated with intestinal ischemia, colonic necrosis, and doubling of risk for serious gastrointestinal adverse events 1
- Variable and inconsistent onset of action 1
Additional Chronic Management Options
Loop or thiazide diuretics: 1
Fludrocortisone: 1
- Increases potassium excretion but carries significant risks 1
- Risks: fluid retention, hypertension, vascular injury 1
- Use cautiously and only when other options are exhausted 1
Monitoring Protocol
Initial monitoring when starting or escalating RAAS inhibitors: 1
- Check potassium within 1 week of starting or escalating doses 1
- Reassess 7-10 days after dose changes 1
After initiating potassium binder therapy: 1
- Reassess potassium 7-10 days after initiation 1
- Monitor closely for both efficacy and hypokalemia (which may be more dangerous than hyperkalemia) 1
High-risk patients requiring more frequent monitoring: 1
For hemodialysis patients: 1
- Target predialysis potassium of 4.0-5.5 mEq/L to minimize mortality risk 1
- Monitor for rebound hyperkalemia every 2-4 hours initially after dialysis if severe initial hyperkalemia (>6.5 mEq/L) 1
Special Population Considerations
Patients with Chronic Kidney Disease
Optimal potassium ranges vary by CKD stage: 1
- Stage 1-2 CKD: 3.5-5.0 mEq/L 1
- Stage 4-5 CKD: 3.3-5.5 mEq/L (broader range due to compensatory mechanisms) 1
- Target for all stages: 4.0-5.0 mEq/L minimizes mortality risk 1
Maintain RAAS inhibitors aggressively in proteinuric CKD using potassium binders—these drugs slow CKD progression. 1
Patients with Cardiovascular Disease
Patients on RAAS inhibitors require careful monitoring: 1
- Assessment 7-10 days after starting or increasing doses 1
- High "normal" potassium concentrations (>5.0 mEq/L) may be associated with adverse outcomes 1
The triple combination of ACE inhibitor + ARB + MRA is NOT recommended due to excessive hyperkalemia risk. 1
Hemodialysis Patients
First-line agent - Sodium zirconium cyclosilicate: 1
- Start with 5g once daily on non-dialysis days 1
- Adjust weekly in 5g increments based on predialysis potassium 1
- Target predialysis potassium 4.0-5.0 mEq/L 1
Second-line agent - Patiromer: 1
- Start with 8.4g once daily with food 1
- Titrate up to 16.8g or 25.2g daily based on response 1
- Monitor magnesium levels closely 1
Consider adjusting dialysate potassium concentration (typically 2.0-3.0 mEq/L) based on predialysis levels, but monitor for intradialytic arrhythmias. 1
Dietary Considerations
Dietary potassium restriction should be approached cautiously: 1
- Evidence linking dietary potassium intake to serum levels is limited 1
- Potassium-rich diet provides cardiovascular benefits, including blood pressure reduction 1
- Newer potassium binders may allow for less restrictive dietary potassium restrictions 1
Avoid potassium supplements and salt substitutes (which have high potassium content). 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
Do not rely solely on ECG findings—they are highly variable and less sensitive than laboratory tests. 1
Do not use sodium bicarbonate in patients without metabolic acidosis—it is only indicated when acidosis is present (pH <7.35, bicarbonate <22 mEq/L). 1
Never give insulin without glucose—hypoglycemia can be life-threatening. 1
Remember that calcium, insulin, and beta-agonists are temporizing measures only—they do NOT remove potassium from the body. 1 Failure to initiate concurrent potassium-lowering therapies will result in recurrent life-threatening arrhythmias within 30-60 minutes. 1
Avoid amiloride and triamterene when using mineralocorticoid receptor antagonists due to increased hyperkalemia risk. 1
Team Approach
Optimal chronic hyperkalemia management involves a multidisciplinary team: 1