Immediate Treatment for Hyperkalemia
For hyperkalemia, immediately stabilize the cardiac membrane with IV calcium, shift potassium into cells with insulin/glucose and albuterol, then eliminate potassium from the body using diuretics, potassium binders, or hemodialysis—all while addressing the underlying cause. 1, 2
Step 1: Assess Severity and ECG Changes
Obtain an ECG immediately, as ECG changes indicate urgent treatment regardless of the absolute potassium level. 1, 2
- Severe hyperkalemia: Potassium ≥6.5 mEq/L is life-threatening 1, 2
- Moderate hyperkalemia: Potassium 6.0-6.4 mEq/L 1, 2
- Mild hyperkalemia: Potassium 5.0-5.9 mEq/L 1, 2
ECG changes requiring immediate treatment include: peaked T waves, flattened P waves, prolonged PR interval, and widened QRS complex 1, 2. These findings mandate urgent intervention even if potassium levels are not yet available 2.
Critical pitfall: Absent or atypical ECG changes do not exclude the necessity for immediate intervention—do not delay treatment while waiting for repeat lab confirmation if ECG changes are present 2, 3.
Step 2: Cardiac Membrane Stabilization (Immediate Effect: 1-3 Minutes)
Administer IV calcium first if potassium >6.5 mEq/L OR any ECG changes are present. 1, 2
- Calcium gluconate (10%): 15-30 mL IV over 2-5 minutes (preferred for peripheral access) 1, 2
- Calcium chloride (10%): 5-10 mL (500-1000 mg) IV over 2-5 minutes (more rapid effect, requires central line when possible) 1, 2
Onset: 1-3 minutes 1, 2
Duration: 30-60 minutes (temporary) 1, 2
Monitor ECG continuously during administration. If no improvement within 5-10 minutes, repeat the dose 1, 2. Calcium does NOT lower serum potassium—it only stabilizes cardiac membranes temporarily. 1, 2
Administration caution: Calcium chloride should be given through a central line when possible, as extravasation can cause severe tissue injury 1. Stop injection if symptomatic bradycardia occurs 1.
Step 3: Shift Potassium Into Cells (Effect Within 15-30 Minutes)
Administer all three agents together for maximum effect: 2
Insulin with Glucose (First-Line)
- Insulin regular: 10 units IV push 1, 2
- Dextrose 50% (D50W): 50 mL (25g glucose) IV over 15-30 minutes 1, 2
- Onset: 15-30 minutes 1, 2
- Duration: 4-6 hours 1, 2
- Effect: Lowers potassium by 0.5-1.2 mEq/L 1
Critical safety: Always give glucose with insulin to prevent life-threatening hypoglycemia 1, 2. Monitor glucose levels closely, especially in patients with low baseline glucose, no diabetes, female sex, or altered renal function 1.
Nebulized Albuterol (Adjunctive)
- Albuterol: 10-20 mg nebulized over 15 minutes 1, 2
- Onset: 15-30 minutes 1, 2
- Duration: 2-4 hours 1, 2
- Effect: Lowers potassium by 0.5-1.0 mEq/L 2
Sodium Bicarbonate (Only if Metabolic Acidosis Present)
- Sodium bicarbonate: 50 mEq IV over 5 minutes 1, 2
- Indication: ONLY use if concurrent metabolic acidosis (pH <7.35, bicarbonate <22 mEq/L) 1, 2
- Onset: 30-60 minutes 2
Critical pitfall: Do NOT use sodium bicarbonate without metabolic acidosis—it is ineffective and wastes time 2. Bicarbonate is not efficacious as monotherapy 3.
Step 4: Eliminate Potassium From the Body (Longer-Term Effect)
Loop Diuretics (If Adequate Renal Function)
Potassium Binders (Preferred for Chronic Management)
Sodium zirconium cyclosilicate (SZC/Lokelma): 10g three times daily for 48 hours, then 5-15g once daily for maintenance 1, 2
Patiromer (Veltassa): 8.4g once daily, titrated up to 25.2g daily 1, 2, 4
Avoid sodium polystyrene sulfonate (Kayexalate): Delayed onset, limited efficacy, and risk of bowel necrosis 1, 2, 5.
Hemodialysis (Most Effective Method)
- Hemodialysis is the most reliable and effective method for severe hyperkalemia, especially in patients with renal failure, oliguria, or cases unresponsive to medical management 1, 2, 6, 5.
Step 5: Prevent Rebound Hyperkalemia
Temporary measures (insulin/glucose, albuterol) provide only transient effects (1-4 hours), and rebound hyperkalemia can occur after 2 hours. 1
- Monitor potassium levels every 2-4 hours during acute treatment 1, 2
- Initiate potassium-lowering agents early to prevent rebound 1
- Review and adjust medications: ACE inhibitors, ARBs, mineralocorticoid receptor antagonists (MRAs), NSAIDs, potassium-sparing diuretics, beta-blockers, potassium supplements, and salt substitutes 1, 2
Step 6: Address Underlying Cause
For patients on RAAS inhibitors with hyperkalemia >5.0 mEq/L: Initiate an approved potassium-lowering agent, closely monitor potassium levels, and maintain RAAS inhibitor therapy unless alternative treatable etiology is identified 1, 2.
For severe hyperkalemia (>6.5 mEq/L) in patients on RAAS inhibitors: Discontinue or reduce RAAS inhibitor temporarily, initiate potassium-lowering agent when levels >5.0 mEq/L, and monitor potassium levels closely 1, 2.
Do NOT permanently discontinue RAAS inhibitors in patients with cardiovascular disease or proteinuric CKD—these medications provide mortality benefit and slow disease progression. Use potassium binders to enable continuation of life-saving therapy 1, 2, 5.
Critical Pitfalls to Avoid
- Never delay calcium administration while waiting for repeat potassium levels if ECG changes are present 2
- Never give insulin without glucose—hypoglycemia can be life-threatening 1, 2
- Never use sodium bicarbonate without metabolic acidosis—it is ineffective 2, 3
- Remember that calcium, insulin, and beta-agonists do NOT remove potassium from the body—they only temporize 1, 2, 6
- Failure to initiate potassium removal strategies will result in recurrent life-threatening hyperkalemia within hours 2