What is the treatment for hyperkalemia?

Treatment of Hyperkalemia

Hyperkalemia treatment follows a three-step algorithmic approach: (1) immediate cardiac membrane stabilization with intravenous calcium, (2) rapid intracellular potassium shift using insulin/glucose and beta-2 agonists, and (3) elimination of potassium from the body through diuretics, potassium binders, or hemodialysis—with treatment intensity determined by potassium level, ECG changes, and symptom severity. 1

Severity Classification and Treatment Triggers

The severity of hyperkalemia dictates treatment urgency and intensity:

• Mild hyperkalemia: 5.0-5.9 mEq/L 1
• Moderate hyperkalemia: 6.0-6.4 mEq/L 1
• Severe hyperkalemia: ≥6.5 mEq/L, which is life-threatening 1

ECG changes (peaked T waves, flattened P waves, prolonged PR interval, widened QRS) mandate urgent treatment regardless of the absolute potassium level. 1 These cardiac manifestations indicate imminent risk of fatal arrhythmias and sudden death. 2

Critical First Step: Rule Out Pseudohyperkalemia

Before initiating aggressive treatment, exclude pseudohyperkalemia from hemolysis or improper blood sampling technique. 1 If suspected, repeat measurement with proper technique or obtain an arterial sample. 2 However, do not delay treatment of severe hyperkalemia while waiting for confirmatory labs if clinical suspicion is high and ECG changes are present. 3

Step 1: Cardiac Membrane Stabilization (Immediate Effect)

For severe hyperkalemia (≥6.5 mEq/L) or any hyperkalemia with ECG changes, immediately administer intravenous calcium to protect against fatal arrhythmias. 1

Calcium Administration Options:

• Calcium chloride (10%): 5-10 mL (500-1000 mg) IV over 2-5 minutes 1

  • Provides more rapid increase in ionized calcium than calcium gluconate 1
  • Preferred in critically ill patients 1
  • Must be given through central venous catheter when possible, as peripheral extravasation causes severe tissue injury 1

• Calcium gluconate (10%): 15-30 mL IV over 2-5 minutes 1

  • Alternative when central access unavailable 1

Monitor heart rate during calcium administration and stop if symptomatic bradycardia develops. 1 The effect begins within minutes but is temporary, lasting only 30-60 minutes. 1 Critically, calcium does not lower serum potassium—it only protects the heart from arrhythmias while other measures take effect. 1

Step 2: Shift Potassium into Cells (Effect Within 15-30 Minutes)

After cardiac stabilization, rapidly shift potassium intracellularly using multiple agents simultaneously:

Insulin with Glucose (Primary Agent):

• 10 units regular insulin IV with 25g glucose (50 mL of D50W) over 15-30 minutes 1
• Onset: 15-30 minutes; duration: 4-6 hours 1
• Monitor blood glucose closely to prevent hypoglycemia 1

Nebulized Beta-2 Agonists:

• Albuterol 10-20 mg nebulized over 15 minutes 1
• Can reduce serum potassium by approximately 0.5-1.0 mEq/L 1
• Onset: 15-30 minutes; duration: 4-6 hours 1
• Use in combination with insulin/glucose for additive effect 1

Sodium Bicarbonate:

• 50 mEq IV over 5 minutes 1
• Most effective in patients with concurrent metabolic acidosis 1
• Less reliable as monotherapy in patients without acidosis 1

Critical Caveat: Rebound Hyperkalemia

All intracellular shift therapies provide only temporary effects (1-4 hours), and rebound hyperkalemia can occur after 2 hours. 1 Therefore, potassium-lowering agents must be initiated early to prevent rebound. 1 Close monitoring of potassium levels during treatment is essential to avoid overcorrection and hypokalemia. 1

Step 3: Eliminate Potassium from Body (Longer-Term Effect)

Loop Diuretics:

• Furosemide 40-80 mg IV 1
• Only effective in patients with adequate renal function 1
• Increases renal potassium excretion 1

Potassium Binders:

Traditional Cation Exchange Resins:

• Sodium polystyrene sulfonate (Kayexalate): 15-50 g orally or rectally with sorbitol 1
• FDA-approved for hyperkalemia treatment but NOT for emergency use due to delayed onset of action 4
• Reserved for subacute treatment 5

Newer Potassium Binders (Preferred):

• Patiromer and sodium zirconium cyclosilicate are safer alternatives to traditional resins 1
• Should be initiated early in patients on RAAS inhibitors with hyperkalemia >5.0 mEq/L to maintain life-saving cardiac medications 1, 3

Hemodialysis:

• Most effective method for severe hyperkalemia, especially in patients with renal failure 1
• Indicated for refractory cases unresponsive to medical treatment 1, 6
• Should be considered early in patients with advanced CKD and severe hyperkalemia 1

Management of Chronic/Recurrent Hyperkalemia

For patients on RAAS inhibitors (ACE inhibitors, ARBs, mineralocorticoid receptor antagonists) with hyperkalemia >5.0 mEq/L, initiate an approved potassium-lowering agent, monitor potassium levels closely, and maintain RAAS inhibitor therapy unless an alternative treatable etiology is identified. 1

This approach is critical because RAAS inhibitors reduce mortality and morbidity in heart failure with reduced ejection fraction, hypertension, coronary artery disease, and chronic kidney disease with Class IA recommendation. 2 Discontinuing these life-saving medications permanently is a major pitfall—instead, reduce dose and add potassium binders. 3

Medication Review:

Identify and adjust drugs that increase potassium levels: 2

• RAAS inhibitors (ACE inhibitors, ARBs, MRAs, aliskiren)
• Potassium-sparing diuretics (spironolactone, amiloride, triamterene)
• NSAIDs
• Beta-blockers
• Trimethoprim-sulfamethoxazole
• Heparin
• Calcineurin inhibitors (cyclosporine, tacrolimus)

Dietary Modifications:

• Restrict potassium intake to <3 g/day 3
• Avoid high-potassium foods: bananas, oranges, melons, potatoes, tomatoes, salt substitutes 3
• Counsel on herbal supplements that may contain potassium 2

Monitoring Strategy:

• Recheck potassium within 24-48 hours after initial intervention 3
• Monitor within 1 week after RAAS inhibitor dose adjustment 3
• Establish individualized monitoring based on comorbidities (CKD, diabetes, heart failure) and medication regimen 3

Hospital Admission Criteria

Admit patients with any of the following: 3

• Severe hyperkalemia (>6.0 mEq/L) regardless of symptoms
• Any ECG changes (peaked T waves, flattened P waves, prolonged PR, widened QRS)
• Symptomatic hyperkalemia (muscle weakness, paresthesias)
• High-risk comorbidities: advanced CKD, heart failure, diabetes mellitus

Common Pitfalls to Avoid

1. Failing to obtain ECG immediately in any patient with hyperkalemia 3
2. Delaying treatment while waiting for repeat labs when ECG changes are present 3
3. Permanently discontinuing RAAS inhibitors instead of dose-reducing and adding potassium binders 3
4. Overlooking pseudohyperkalemia from hemolysis or poor sampling technique 3
5. Failing to initiate potassium elimination measures early, leading to rebound hyperkalemia after temporary shift therapies wear off 1
6. Administering calcium chloride through peripheral IV without recognizing extravasation risk 1
7. Not monitoring glucose after insulin administration, risking hypoglycemia 1