What is the treatment for sudden hyperkalemia?

Treatment of Sudden Hyperkalemia

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

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

This is your first priority because it prevents fatal arrhythmias without waiting for potassium levels to drop.

• Administer calcium chloride 10%: 5-10 mL (500-1000 mg) IV over 2-5 minutes 3, 1
• Alternative: calcium gluconate 10%: 15-30 mL IV over 2-5 minutes if calcium chloride unavailable 3, 1
• Calcium chloride is preferred over calcium gluconate because it provides more rapid increase in ionized calcium concentration, making it more effective in critically ill patients 1
• Effects begin within 1-3 minutes but last only 30-60 minutes 1, 2
• Critical caveat: Calcium does NOT lower potassium levels—it only protects the heart temporarily 1, 4
• Administer through central line when possible, as peripheral extravasation causes severe tissue injury 1
• Monitor heart rate during infusion and stop if symptomatic bradycardia occurs 1

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

These therapies provide temporary reduction in serum potassium while definitive treatments take effect.

Insulin with Glucose (Primary Agent)

• Administer 10 units regular insulin IV with 25g glucose (50 mL of D50W) over 15-30 minutes 3, 1, 2
• Onset of action: 15-30 minutes; duration: 4-6 hours 1, 2
• Can be repeated every 4-6 hours if hyperkalemia persists, with careful glucose and potassium monitoring 4
• Critical pitfall: Monitor glucose closely to prevent hypoglycemia, especially in patients with low baseline glucose, females, altered renal function, or non-diabetics 4

Nebulized Beta-2 Agonist (Adjunctive)

• Administer albuterol 10-20 mg nebulized over 15 minutes 3, 1, 2
• Reduces serum potassium by approximately 0.5-1.0 mEq/L 1
• Use as adjunct to insulin/glucose, not as sole therapy 1, 2

Sodium Bicarbonate (Only If Metabolic Acidosis Present)

• Administer 50 mEq IV over 5 minutes ONLY if concurrent metabolic acidosis exists (pH <7.35, bicarbonate <22 mEq/L) 3, 1, 4
• Effects take 30-60 minutes to manifest 4
• Do not use in patients without acidosis—it is ineffective and potentially harmful 4

Step 3: Eliminate Potassium From Body (Definitive Treatment)

Critical understanding: Steps 1 and 2 are temporizing measures only. Rebound hyperkalemia occurs after 2-4 hours if potassium is not eliminated from the body. 1, 4

For Patients With Adequate Renal Function

• Furosemide 40-80 mg IV to increase renal potassium excretion 3, 1, 2
• Only effective if kidney function preserved 1, 2

For Subacute Management

• Newer potassium binders (patiromer or sodium zirconium cyclosilicate) are preferred over traditional cation exchange resins 1, 2, 4
• Traditional sodium polystyrene sulfonate (Kayexalate) 15-50g orally or rectally can be used but has delayed onset 3
• FDA warning: Neither polystyrene sulfonate nor sodium zirconium cyclosilicate should be used as emergency treatment due to delayed onset of action 5, 6

For Severe or Refractory Cases

• Hemodialysis is the most effective and reliable method for potassium removal, especially in renal failure, oliguria, or cases unresponsive to medical management 3, 1, 2, 4
• Should be initiated during CPR if conventional therapies fail in cardiac arrest from hyperkalemia 7

Special Considerations for Cardiac Arrest

When cardiac arrest occurs secondary to hyperkalemia:

• Continue standard ACLS protocols while administering adjuvant therapies (calcium, insulin/glucose, albuterol) 3
• Consider hemodialysis during CPR if conventional treatments fail after 20 minutes 7
• Prolonged resuscitation efforts are justified because hyperkalemia is reversible 7

Critical Pitfalls to Avoid

• Do not rely solely on ECG findings—they are highly variable and less sensitive than laboratory values 4
• Exclude pseudohyperkalemia from hemolysis or poor phlebotomy technique before initiating aggressive treatment 4
• Remember that calcium, insulin, and beta-agonists do NOT remove potassium—they only temporize 4
• Monitor for rebound hyperkalemia after 2-4 hours when temporary measures wear off 1, 4
• Always administer glucose with insulin to prevent life-threatening hypoglycemia 4

Monitoring Protocol

• Check potassium levels every 2-4 hours after initial treatment 4
• Continuous cardiac monitoring for ECG changes 3, 1
• Monitor glucose levels closely when using insulin 4
• Reassess need for repeat doses of temporizing agents every 4-6 hours 4

Management of Patients on RAAS Inhibitors

• For chronic hyperkalemia >5.0 mEq/L in patients requiring RAAS inhibitors, initiate potassium-lowering agent and maintain RAAS inhibitor therapy rather than discontinuing 1, 2, 4
• Only discontinue or reduce RAAS inhibitors temporarily if K+ >6.5 mEq/L 4
• This approach maintains cardiovascular benefits while managing hyperkalemia 1