What is the treatment for hyperkalemia?

Treatment of Hyperkalemia

For acute hyperkalemia with potassium ≥6.5 mEq/L or any ECG changes, immediately administer IV calcium gluconate 15-30 mL (or calcium chloride 5-10 mL) over 2-5 minutes, followed simultaneously by insulin 10 units with 25g dextrose (50 mL D50W) and nebulized albuterol 10-20 mg—this three-pronged approach provides cardiac protection within 1-3 minutes and shifts potassium intracellularly within 15-30 minutes. 1, 2

Initial Assessment

Before initiating aggressive treatment, verify the result is not pseudohyperkalemia from hemolysis, repeated fist clenching, or poor phlebotomy technique by repeating with proper technique or arterial sampling 2, 3. Obtain an ECG immediately—peaked T waves, flattened P waves, prolonged PR interval, or widened QRS indicate urgent treatment regardless of the potassium level 1, 2.

Severity Classification:

• Mild: 5.0-5.9 mEq/L 1, 2
• Moderate: 6.0-6.4 mEq/L 1, 2
• Severe: ≥6.5 mEq/L (life-threatening) 1, 2

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

Administer IV calcium immediately if potassium >6.5 mEq/L OR any ECG changes are present 1, 2, 3:

• Calcium gluconate (10%): 15-30 mL IV over 2-5 minutes 1, 2
• Calcium chloride (10%): 5-10 mL (500-1000 mg) IV over 2-5 minutes (preferred in critically ill patients as it provides more rapid increase in ionized calcium) 1, 2

Critical considerations:

• Calcium does NOT lower serum potassium—it only stabilizes cardiac membranes temporarily for 30-60 minutes 1, 2
• Calcium chloride should be administered through a central line when possible due to risk of severe tissue injury with extravasation 1
• Monitor heart rate during administration and stop if symptomatic bradycardia occurs 1
• Repeat dosing may be necessary if no ECG improvement within 5-10 minutes 2
• In patients with malignant hyperthermia, use calcium only in extremis due to risk of myoplasmic calcium overload 2

Step 2: Shift Potassium into Cells (Onset 15-30 Minutes, Duration 4-6 Hours)

Give all three agents together for maximum effect 2:

Insulin with Glucose (First-Line)

• Standard dose: 10 units regular insulin IV with 25g glucose (50 mL of D50W) over 15-30 minutes 1, 2
• Alternative: Some protocols use 0.1 units/kg (approximately 5-7 units in adults) 2
• Pediatric dose: Use D10W at 200 mg/kg or D25W (100 mL provides 25g glucose) 1
• Never give insulin without glucose—hypoglycemia can be life-threatening 2
• Verify potassium is not below 3.3 mEq/L before administering insulin 2
• Can be repeated every 4-6 hours if hyperkalemia persists, with careful monitoring of glucose and potassium every 2-4 hours 2
• Patients at higher risk for hypoglycemia: low baseline glucose, no diabetes, female sex, altered renal function 2

Beta-2 Agonists (Adjunctive)

• Nebulized albuterol: 10-20 mg over 15 minutes 1, 2
• Nebulized salbutamol: 10-20 mg over 15 minutes (alternative) 2, 4
• Reduces serum potassium by approximately 0.5-1.0 mEq/L 1
• Effects last 2-4 hours 2

Sodium Bicarbonate (ONLY if Metabolic Acidosis Present)

• Dose: 50 mEq IV over 5 minutes 1, 2
• Use ONLY when: pH <7.35 and bicarbonate <22 mEq/L 2
• Do not use without metabolic acidosis—it is ineffective and wastes time 2
• Effects take 30-60 minutes to manifest 2

Critical pitfall: Remember that calcium, insulin, and beta-agonists are temporizing measures only—they do NOT remove potassium from the body 2, 3. Rebound hyperkalemia can occur after 2 hours 1.

Step 3: Eliminate Potassium from Body (Definitive Treatment)

Acute Setting

Loop Diuretics (If Adequate Renal Function):

• Furosemide: 40-80 mg IV 1, 2
• Effective only in patients with adequate kidney function 1, 2
• Titrate to maintain euvolemia, not primarily for potassium management 2

Hemodialysis (Most Effective Method):

• Most reliable and effective method for severe hyperkalemia 1, 2, 5
• Reserved for: severe cases unresponsive to medical management, oliguria, or end-stage renal disease 2
• Monitor for rebound hyperkalemia within 4-6 hours post-dialysis as intracellular potassium redistributes 2

Chronic/Subacute Management

Newer Potassium Binders (Preferred):

Sodium zirconium cyclosilicate (SZC/Lokelma):

• Acute phase: 10g three times daily for 48 hours 1, 2
• Maintenance: 5-15g once daily 1, 2
• Onset: ~1 hour (suitable for urgent scenarios) 1, 2
• Hemodialysis patients: 5g once daily on non-dialysis days, adjust weekly in 5g increments 2
• FDA indication: Treatment of hyperkalemia in adults, but NOT for emergency life-threatening hyperkalemia due to delayed onset 6
• Monitor for edema due to sodium content 2

Patiromer (Veltassa):

• Starting dose: 8.4g once daily with food 1, 2
• Titration: Up to 25.2g daily based on potassium levels 1, 2
• Onset: ~7 hours 1, 2
• Administration: Separate from other oral medications by at least 3 hours (6 hours in gastroparesis) 7
• Monitor magnesium levels—causes hypomagnesemia and hypercalcemia 2

Sodium Polystyrene Sulfonate (Kayexalate) - AVOID:

• Do NOT use for acute management 2, 7
• Significant limitations: delayed onset, risk of intestinal necrosis and bowel perforation (especially with sorbitol), doubling of serious GI adverse events 2
• FDA indication: Treatment of hyperkalemia, but NOT for emergency life-threatening hyperkalemia 7
• If used: 15-50g orally or rectally, but newer agents strongly preferred 1

Medication Management During Acute Episode

Temporarily discontinue or reduce 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

Chronic Hyperkalemia Prevention

For patients on RAAS inhibitors with K+ 5.0-6.5 mEq/L 1, 2:

• Initiate patiromer or SZC while maintaining RAAS inhibitor therapy 1, 2
• Do NOT permanently discontinue RAAS inhibitors in patients with cardiovascular disease or proteinuric CKD—they provide mortality benefit and slow disease progression 2

For patients with K+ >6.5 mEq/L 1, 2:

• Temporarily discontinue or reduce RAAS inhibitor
• Initiate potassium binder when levels >5.0 mEq/L
• Restart RAAS inhibitor at lower dose once K+ <5.0-5.5 mEq/L with concurrent potassium binder 2

Additional measures:

• Optimize loop or thiazide diuretics to promote urinary potassium excretion 2
• Correct metabolic acidosis if present 8
• Dietary modification: reduce nonplant sources of potassium rather than restricting all potassium-rich foods (potassium-rich diets have cardiovascular benefits) 2, 8

Monitoring Protocol

Acute phase:

• Check potassium every 2-4 hours after initial treatment 2
• Continuous cardiac monitoring mandatory during calcium administration 2
• Monitor glucose closely to avoid hypoglycemia with insulin 2

Chronic management:

• Check potassium within 1 week of starting or escalating RAAS inhibitors 2, 3
• Reassess 7-10 days after initiating potassium binder therapy 2
• High-risk patients (CKD, heart failure, diabetes, history of hyperkalemia) require more frequent monitoring 2, 3

Target potassium levels:

• General population: 3.5-5.0 mEq/L 2
• Advanced CKD (stage 4-5): 3.3-5.5 mEq/L (broader range tolerated) 2
• Hemodialysis patients: predialysis 4.0-5.5 mEq/L to minimize mortality 2

Critical Pitfalls to Avoid

• Never delay treatment while waiting for repeat lab confirmation if ECG changes are present 2
• Do not rely solely on ECG findings—they are highly variable and less sensitive than laboratory tests 2, 3
• Never use sodium bicarbonate without metabolic acidosis—it is ineffective 2
• Never give insulin without glucose 2, 3
• Remember that temporary measures (calcium, insulin, beta-agonists) do NOT remove potassium—definitive elimination strategies must follow 2, 3
• Avoid sodium polystyrene sulfonate due to serious safety concerns 2, 7
• Do not permanently discontinue RAAS inhibitors in cardiovascular disease or proteinuric CKD—use potassium binders instead 2