What are the steps for managing hyperkalemia?

Management of Hyperkalemia

Severity Classification and Initial Assessment

Hyperkalemia should be classified immediately as mild (5.0-5.5 mEq/L), moderate (5.5-6.0 mEq/L), or severe (>6.0 mEq/L), with treatment urgency determined by both the potassium level and presence of ECG changes. 1, 2

• Obtain an ECG immediately in all patients with potassium >5.5 mEq/L to assess for peaked T waves, flattened P waves, prolonged PR interval, or widened QRS complex 1, 3
• ECG changes indicate urgent treatment regardless of the absolute potassium level 1, 3
• Rule out pseudohyperkalemia from hemolysis, repeated fist clenching, or poor phlebotomy technique by repeating the measurement with proper technique 1, 3
• Absent or atypical ECG changes do not exclude the necessity for immediate intervention in severe hyperkalemia 4

Emergency Management of Severe Hyperkalemia (>6.0 mEq/L or Any ECG Changes)

For severe hyperkalemia or any ECG changes, immediately administer intravenous calcium for cardiac membrane stabilization, followed by agents to shift potassium intracellularly, then initiate potassium removal from the body. 1, 2

Step 1: Cardiac Membrane Stabilization (Immediate - Within 1-3 Minutes)

• Administer calcium gluconate 10%: 15-30 mL (1.5-3 grams) IV over 2-5 minutes 1, 3
• Alternative: calcium chloride 10%: 5-10 mL IV over 2-5 minutes (use central line if possible due to tissue injury risk) 1, 3
• Effects begin within 1-3 minutes but last only 30-60 minutes 2, 3
• Calcium does NOT lower potassium—it only stabilizes cardiac membranes temporarily 3
• Repeat dosing may be necessary if no ECG improvement within 5-10 minutes 3
• Continuous cardiac monitoring is mandatory during and after administration 3

Step 2: Shift Potassium Intracellularly (Onset 15-30 Minutes)

Administer all three agents together for maximum effect: 3

• Insulin 10 units regular IV plus 25 grams dextrose (50 mL of 50% dextrose) 1, 2, 4

  • Onset within 15-30 minutes, effects last 4-6 hours 2, 3
  • Monitor glucose closely to prevent hypoglycemia 3
  • Can be repeated every 4-6 hours as needed 3
  • Patients with low baseline glucose, no diabetes, female sex, and altered renal function are at higher risk of hypoglycemia 3

• Nebulized albuterol 10-20 mg in 4 mL 1, 3, 4

  • Effects last 2-4 hours 3
  • Use as adjunctive therapy to insulin 3

• Sodium bicarbonate 50 mEq IV over 5 minutes ONLY if metabolic acidosis is present (pH <7.35, bicarbonate <22 mEq/L) 1, 2, 3

  • Effects take 30-60 minutes to manifest 3
  • Do not use without metabolic acidosis—it is ineffective and wastes time 3

Step 3: Remove Potassium from the Body

Choose based on renal function and clinical context: 3

• Loop diuretics (furosemide 40-80 mg IV) for patients with adequate kidney function (eGFR >30 mL/min/1.73m²) 1, 2, 3

  • Increases renal potassium excretion by stimulating flow to renal collecting ducts 3
  • Titrate to maintain euvolemia, not primarily for potassium management 3

• Hemodialysis is the most effective and reliable method for severe hyperkalemia 1, 2, 3, 5

  • Reserved for severe cases unresponsive to medical management, oliguria, or end-stage renal disease 3
  • Monitor for rebound hyperkalemia 2-4 hours post-dialysis as intracellular potassium redistributes 1, 3

• Newer potassium binders (preferred over sodium polystyrene sulfonate): 2, 3

  • Sodium zirconium cyclosilicate (SZC/Lokelma): 10 g three times daily for 48 hours, then 5-15 g once daily for maintenance (onset ~1 hour) 2, 3
  • Patiromer (Veltassa): 8.4 g once daily with food, titrated up to 25.2 g daily (onset ~7 hours) 2, 3

Step 4: Medication Review During Acute Episode

Temporarily discontinue or reduce the following medications: 3

• RAAS inhibitors (ACE inhibitors, ARBs, mineralocorticoid antagonists) if K+ >6.5 mEq/L 1, 2, 3
• NSAIDs 1, 3
• Potassium-sparing diuretics (spironolactone, amiloride, triamterene) 3
• Trimethoprim 3
• Heparin 2, 3
• Beta-blockers 3
• Potassium supplements and salt substitutes 1, 3

Management of Moderate Hyperkalemia (5.5-6.0 mEq/L) Without ECG Changes

For moderate hyperkalemia without ECG changes, focus on shifting potassium intracellularly and initiating potassium removal, while avoiding cardiac membrane stabilization unless ECG changes develop. 1

• Do NOT administer calcium gluconate unless ECG changes are present 3
• Consider insulin with glucose and/or nebulized albuterol if potassium is approaching 6.0 mEq/L 1
• Initiate loop diuretics if adequate renal function (eGFR >30 mL/min/1.73m²) 1, 3
• Start potassium binder therapy (patiromer or sodium zirconium cyclosilicate) 2, 3
• Restrict potassium intake to <3 g/day (50-70 mmol/day) 1
• Recheck potassium within 24-48 hours 1
• Immediate hospital referral is indicated if potassium rises above 6.0 mEq/L, ECG changes develop, or symptoms appear 1

Management of Mild Hyperkalemia (5.0-5.5 mEq/L)

For mild hyperkalemia, focus on identifying and addressing underlying causes rather than initiating acute interventions. 3

• Do NOT initiate acute interventions (calcium, insulin, albuterol) for mild hyperkalemia without ECG changes or symptoms 3
• Review and adjust medications that contribute to hyperkalemia 1, 3
• Restrict potassium intake to <3 g/day, avoiding high-potassium foods (bananas, oranges, potatoes, tomatoes, salt substitutes, legumes, chocolate, yogurt) 1
• Consider loop diuretics if adequate renal function 1, 3
• Recheck potassium within 1 week 1

Chronic Hyperkalemia Management and Prevention of Recurrence

After acute resolution, the priority is preventing recurrence while maintaining beneficial RAAS inhibitor therapy using potassium binders rather than permanently discontinuing these life-saving medications. 1, 2, 3

Medication Optimization

• Do NOT permanently discontinue RAAS inhibitors—they provide mortality benefit in heart failure, hypertension, and chronic kidney disease 1, 2, 3, 6
• For patients with K+ 5.0-6.5 mEq/L on RAAS inhibitors: initiate potassium binder and maintain RAAS inhibitor therapy 2, 3
• For patients with K+ >6.5 mEq/L: temporarily hold or reduce RAAS inhibitor, then restart at lower dose once K+ <5.0 mEq/L with concurrent potassium binder 2, 3
• Eliminate or reduce contributing medications: NSAIDs, trimethoprim, heparin, beta-blockers, potassium supplements, salt substitutes 1, 3

Potassium Binder Selection

Newer potassium binders (patiromer and sodium zirconium cyclosilicate) are preferred over sodium polystyrene sulfonate due to superior safety profile. 2, 3

• Patiromer (Veltassa): 8.4 g once daily with food, titrated up to 25.2 g daily based on potassium levels 2, 3

  • Separate from other oral medications by at least 3 hours 3
  • Onset of action ~7 hours 3
  • Binds potassium in exchange for calcium in the colon 3

• Sodium zirconium cyclosilicate (SZC/Lokelma): 10 g three times daily for 48 hours, then 5-15 g once daily for maintenance 2, 3

  • Onset of action ~1 hour, suitable for more urgent scenarios 3
  • Reduces serum potassium within 1 hour of a single 10-g dose 3

• Avoid chronic use of sodium polystyrene sulfonate (Kayexalate) due to risk of bowel necrosis and serious gastrointestinal adverse events 2, 3

Monitoring Protocol

Establish a structured monitoring schedule based on risk factors: 3

• Check potassium within 1 week of starting or escalating RAAS inhibitors 1, 3
• Reassess 7-10 days after initiating potassium binder therapy 3
• For high-risk patients (CKD, heart failure, diabetes, history of hyperkalemia): check every 1-2 weeks initially, then every 3 months, then every 6 months 3
• Monitor closely for hypokalemia in patients on potassium binders, as hypokalemia may be more dangerous than hyperkalemia 3

Dietary Modifications

Dietary potassium restriction should be nuanced, focusing on reducing nonplant sources rather than blanket restriction. 6

• Evidence linking dietary potassium intake to serum levels is limited 3, 6
• A potassium-rich diet provides cardiovascular benefits, including blood pressure reduction 3
• Newer potassium binders may allow less restrictive dietary potassium restrictions 3
• When restriction is necessary, limit to <3 g/day (50-70 mmol/day) and avoid: bananas, oranges, melons, potatoes, tomato products, salt substitutes, legumes, lentils, chocolate, yogurt, certain herbal supplements 1

Special Populations

Chronic Kidney Disease

• Maintain RAAS inhibitors aggressively in proteinuric CKD using potassium binders, as these drugs slow CKD progression 3, 6
• 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 3
• Target potassium of 4.0-5.0 mEq/L minimizes mortality risk 3
• Loop diuretics remain effective with eGFR >30 mL/min/1.73m² 3

Dialysis Patients

• Target predialysis potassium of 4.0-5.5 mEq/L to minimize mortality risk 3
• Consider adjusting dialysate potassium concentration (typically 2.0-3.0 mEq/L) based on predialysis levels 3
• Lower dialysate potassium (2.0 mEq/L) may be needed for recurrent severe hyperkalemia, but monitor for intradialytic arrhythmias 3
• Monitor for rebound hyperkalemia 2-4 hours post-dialysis 3

Critical Pitfalls to Avoid

• Never delay treatment while waiting for repeat lab confirmation if ECG changes are present 3
• Never give insulin without glucose—hypoglycemia can be life-threatening 3
• Never use sodium bicarbonate without metabolic acidosis—it is ineffective 3
• Remember that calcium, insulin, and beta-agonists are temporizing measures only—they do NOT remove potassium from the body 3
• Do not rely solely on ECG findings—they are highly variable and less sensitive than laboratory tests 3
• Do not permanently discontinue beneficial RAAS inhibitors—use dose reduction and potassium binders instead 1, 2, 3
• Do not overlook pseudohyperkalemia from poor phlebotomy technique or delayed sample processing 1, 3
• Do not use chronic sodium polystyrene sulfonate due to risk of bowel necrosis 2, 3