What is the treatment for hyperkalemia?

Treatment for Hyperkalemia

For severe hyperkalemia (≥6.5 mEq/L) or any potassium level with ECG changes, immediately administer intravenous calcium chloride 10% (5-10 mL over 2-5 minutes) to stabilize cardiac membranes, followed within 15 minutes by insulin 10 units with 25g glucose and nebulized albuterol 10-20 mg to shift potassium intracellularly. 1

Severity Classification and Initial Assessment

Before initiating treatment, verify the result is not pseudohyperkalemia from hemolysis, repeated fist clenching, or poor phlebotomy technique 2. Classify severity as:

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

Critical caveat: ECG changes (peaked T waves, flattened P waves, prolonged PR interval, widened QRS) indicate urgent treatment regardless of potassium level 1. However, absent or atypical ECG changes do not exclude the necessity for immediate intervention 3.

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

For severe hyperkalemia or any ECG changes:

• Calcium chloride 10%: 5-10 mL (500-1000 mg) IV over 2-5 minutes - preferred agent 1, 4
• Alternative: Calcium gluconate 10%: 15-30 mL IV over 2-5 minutes 1

Key points about calcium administration:

• Calcium chloride provides more rapid increase in ionized calcium than calcium gluconate, making it more effective in critically ill patients 1
• Administer through central venous catheter when possible, as extravasation through peripheral IV may cause severe tissue injury 1
• Effects begin within 1-3 minutes but last only 30-60 minutes 2, 4
• Does not lower serum potassium - only protects against arrhythmias 1
• Monitor heart rate during administration and stop if symptomatic bradycardia occurs 1
• May repeat dose if no ECG improvement within 5-10 minutes 2

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

Administer the following agents simultaneously for additive effect:

Insulin with Glucose (First-line)

• 10 units regular insulin IV with 25g glucose (50 mL of D50W) over 15-30 minutes 1, 4
• Onset: 15-30 minutes; Duration: 4-6 hours 1
• Critical monitoring: Check glucose levels to prevent hypoglycemia 2
• Patients at higher risk for hypoglycemia: low baseline glucose, no diabetes history, female sex, altered renal function 2
• Can be repeated every 4-6 hours as needed, monitoring potassium every 2-4 hours 2

Nebulized Beta-2 Agonist (Adjunctive)

• Albuterol 10-20 mg nebulized over 15 minutes 1, 4
• Onset: 15-30 minutes; Duration: 2-4 hours 1, 2
• Can reduce serum potassium by approximately 0.5-1.0 mEq/L 1

Sodium Bicarbonate (Only if Metabolic Acidosis Present)

• 50 mEq IV over 5 minutes 1
• Use ONLY in patients with concurrent metabolic acidosis (pH <7.35, bicarbonate <22 mEq/L) 1, 2
• Effects take 30-60 minutes to manifest 2
• Do not use in patients without acidosis - this is a common pitfall 2

Important warning: These temporizing measures provide only transient effects (1-4 hours), and rebound hyperkalemia can occur after 2 hours 1. Definitive potassium removal must be initiated simultaneously.

Step 3: Eliminate Potassium from Body (Definitive Treatment)

Loop Diuretics (If Adequate Renal Function)

• Furosemide 40-80 mg IV 1, 4
• Effective only in patients with preserved kidney function 4
• Increases renal potassium excretion through enhanced distal sodium delivery 2

Potassium Binders

For subacute to chronic management:

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

  • Onset: ~1 hour (fastest-acting binder) 2
  • Reduces serum potassium within 1 hour of single dose 2
  • Effective for both acute (≥5.8 mEq/L) and chronic management 2

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

  • Onset: ~7 hours 2
  • FDA limitation: Should not be used as emergency treatment for life-threatening hyperkalemia due to delayed onset 5

• Sodium polystyrene sulfonate (Kayexalate): 15-50g orally or rectally with sorbitol 1

  • Significant limitations: Delayed onset of action and risk of bowel necrosis 2
  • Should be avoided for acute management 2
  • FDA limitation: Should not be used as emergency treatment due to delayed onset 6

Hemodialysis

• Most effective and reliable method for severe hyperkalemia 1, 4
• Indications: Severe cases unresponsive to medical management, oliguria, end-stage renal disease, or refractory hyperkalemia 2, 3

Treatment Algorithm by Severity

Severe Hyperkalemia (K+ ≥6.5 mEq/L or ECG Changes)

1. Immediate: Calcium chloride 10%: 5-10 mL IV over 2-5 minutes 4
2. Within 15 minutes: Insulin 10 units + glucose 25g IV AND albuterol 10-20 mg nebulized 4
3. Simultaneously: Initiate loop diuretics (if renal function adequate) OR arrange hemodialysis 4
4. Monitor: Potassium every 2-4 hours, continuous cardiac monitoring 2

Moderate Hyperkalemia (K+ 6.0-6.4 mEq/L Without ECG Changes)

1. Insulin/glucose and albuterol for intracellular shift 4
2. Loop diuretics or potassium binders 4
3. Review and eliminate contributing medications 4

Mild Hyperkalemia (K+ 5.0-5.9 mEq/L)

1. Review and discontinue offending medications (NSAIDs, potassium supplements, salt substitutes) 4
2. Initiate potassium binder for chronic management 4
3. Do NOT discontinue RAAS inhibitors - maintain therapy with potassium binders 4
4. Do NOT initiate acute interventions (calcium, insulin, albuterol) without ECG changes or symptoms 2

Special Population: Patients on RAAS Inhibitors

Critical principle: Maintain life-saving RAAS inhibitor therapy (ACE inhibitors, ARBs, mineralocorticoid antagonists) by using potassium-lowering agents rather than discontinuing these medications 2, 4.

For K+ 5.0-6.5 mEq/L:

• Initiate approved potassium-lowering agent (patiromer or SZC) 1, 2
• Maintain RAAS inhibitor therapy unless alternative treatable etiology identified 1, 2
• Monitor potassium closely 1

For K+ >6.5 mEq/L:

• Discontinue or reduce RAAS inhibitor temporarily 1, 2
• Initiate potassium-lowering agent when levels >5.0 mEq/L 1
• Restart RAAS inhibitor at lower dose with concurrent potassium binder therapy once stabilized 2

Monitoring Protocol

• Check potassium within 1 week of starting or escalating RAAS inhibitors 2
• Reassess 7-10 days after initiating potassium binder therapy 2
• For patients on acute treatment: Monitor potassium every 2-4 hours 2
• Higher-risk patients (CKD, heart failure, diabetes) require more frequent monitoring 2
• Monitor for hypokalemia in patients on potassium binders, which may be even more dangerous than hyperkalemia 2

Key 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 - only indicated when acidosis is present 2
• Always administer glucose with insulin to prevent hypoglycemia 2
• Remember that calcium, insulin, and beta-agonists do not remove potassium - they only temporize 2
• Do not permanently discontinue RAAS inhibitors - this leads to worse cardiovascular and renal outcomes 2
• Exclude pseudohyperkalemia before initiating aggressive treatment 1

Chronic Management Considerations

• Eliminate contributing medications: NSAIDs, trimethoprim, heparin, beta-blockers, potassium supplements 2
• Optimize diuretic therapy with loop or thiazide diuretics 2
• Dietary potassium restriction has limited evidence and should be approached cautiously, as potassium-rich diets provide cardiovascular benefits 2
• For advanced CKD (stage 4-5), optimal potassium range is broader: 3.3-5.5 mEq/L 2