What is the treatment for hyperkalemia?

Treatment for High Potassium (Hyperkalemia)

For severe hyperkalemia (≥6.5 mEq/L) or any potassium level with ECG changes, immediately administer intravenous calcium to stabilize the cardiac membrane, followed by insulin with glucose and nebulized beta-agonists to shift potassium into cells, then use definitive removal strategies including diuretics, potassium binders, or hemodialysis. 1, 2

Severity Classification and Initial Assessment

Before initiating treatment, verify the result is not pseudohyperkalemia from hemolysis, repeated fist clenching, or poor phlebotomy technique by repeating the measurement with appropriate technique or arterial sampling. 1, 2

Hyperkalemia severity is classified as:

• 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

ECG changes (peaked T waves, flattened P waves, prolonged PR interval, widened QRS) indicate urgent treatment regardless of potassium level. 1, 2 However, do not rely solely on ECG findings—they are highly variable and less sensitive than laboratory tests. 1

Acute Hyperkalemia Management: Three-Step Approach

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

Administer intravenous calcium first in any patient with severe hyperkalemia or ECG changes:

• Calcium chloride (10%): 5-10 mL (500-1000 mg) IV over 2-5 minutes (preferred in critically ill patients) 1, 2
• Calcium gluconate (10%): 15-30 mL IV over 2-5 minutes (alternative) 1, 2

Calcium chloride provides more rapid increase in ionized calcium concentration than calcium gluconate, making it more effective in critically ill patients. 2 Administer through a central venous catheter when possible, as extravasation through peripheral IV may cause severe tissue injury. 2 Monitor heart rate during administration and stop if symptomatic bradycardia occurs. 2

Critical caveat: Calcium does not lower serum potassium—it only protects against arrhythmias temporarily (30-60 minutes). 1, 2

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

Administer all of the following simultaneously for maximum effect:

• Insulin with glucose: 10 units regular insulin IV with 25g glucose (50 mL of D50W) over 15-30 minutes 1, 2

  • Ensure glucose is administered with insulin to prevent hypoglycemia 1
  • Patients with low baseline glucose, no diabetes, female sex, and altered renal function are at higher risk of hypoglycemia 1
  • Can be repeated every 4-6 hours if hyperkalemia persists, with careful monitoring of potassium and glucose every 2-4 hours 1

• Nebulized beta-2 agonist: Albuterol/salbutamol 10-20 mg nebulized over 15 minutes 1, 2

  • Can be used alone or to augment insulin effect 1
  • Duration of effect is 2-4 hours 1

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

  • Do not use in patients without metabolic acidosis—it is only indicated when acidosis is present 1
  • Effects take 30-60 minutes to manifest 1

Important warning: These measures are temporary and rebound hyperkalemia can occur after 2 hours. 2 Definitive potassium removal must be initiated immediately. 2

Step 3: Eliminate Potassium from Body (Definitive Treatment)

• Loop diuretics: Furosemide 40-80 mg IV to increase renal potassium excretion 1, 2

  • Effective only in patients with adequate kidney function 1, 2

• Potassium binders:

  • Newer agents (preferred): Patiromer or sodium zirconium cyclosilicate for safer long-term management 1, 2
  • Traditional agent: Sodium polystyrene sulfonate (Kayexalate) 15-50 g orally or rectally with sorbitol 1, 2
  • FDA limitation: Sodium polystyrene sulfonate should NOT be used as emergency treatment for life-threatening hyperkalemia due to delayed onset of action 3

• Hemodialysis: The most reliable and effective method for severe hyperkalemia, especially in patients with renal failure, oliguria, or cases unresponsive to medical management 1, 2, 4

Chronic and Recurrent Hyperkalemia Management

For patients on RAAS inhibitors (ACE inhibitors, ARBs, mineralocorticoid antagonists):

• If potassium >5.0 mEq/L: Initiate an approved potassium-lowering agent and maintain RAAS inhibitor therapy unless alternative treatable cause is identified 1, 2

  • Maintaining these life-saving medications by using potassium binders is preferable to discontinuing therapy 2

• If potassium >6.5 mEq/L: Temporarily discontinue or reduce RAAS inhibitor, initiate potassium-lowering agent, and monitor potassium levels closely 1, 2

• Monitoring protocol: Check potassium within 7-10 days after starting or increasing RAAS inhibitor doses 1, 2

  • More frequent monitoring required in high-risk patients with chronic kidney disease, diabetes, heart failure, or history of hyperkalemia 1

Long-term strategies:

• Loop or thiazide diuretics to promote urinary potassium excretion 1, 2
• Review and adjust medications that contribute to hyperkalemia (ACE inhibitors, ARBs, MRAs, NSAIDs, beta-blockers) 1, 2
• Consider fludrocortisone to increase potassium excretion, though it carries risks of fluid retention and hypertension 1

Key Clinical Pitfalls to Avoid

• Do not rely solely on ECG findings—they are highly variable and less sensitive than laboratory tests 1
• Do not use sodium bicarbonate without metabolic acidosis—it is only indicated when acidosis is present 1
• Remember that calcium, insulin, and beta-agonists do not remove potassium—they only temporize, requiring definitive removal strategies 1
• Do not use sodium polystyrene sulfonate for emergency treatment—it has delayed onset of action 3
• Exclude pseudohyperkalemia before initiating aggressive treatment—repeat measurement with proper technique 1, 2

Team Approach

Optimal chronic hyperkalemia management involves specialists (cardiologists, nephrologists), primary care physicians, nurses, pharmacists, social workers, and dietitians working collaboratively. 1