What is the treatment for hyperkalemia?

Treatment of Hyperkalemia

For severe hyperkalemia (K+ ≥6.5 mEq/L or any ECG changes), immediately administer IV calcium for cardiac protection, followed within minutes by insulin with glucose and nebulized albuterol to shift potassium intracellularly, then initiate definitive potassium removal with loop diuretics (if renal function adequate), newer potassium binders, or hemodialysis. 1, 2, 3

Severity Classification

Before initiating treatment, classify the severity:

• Mild hyperkalemia: 5.0-5.9 mEq/L 1, 2
• Moderate hyperkalemia: 6.0-6.4 mEq/L 1, 2
• Severe hyperkalemia: ≥6.5 mEq/L (life-threatening) 1, 2
• ECG changes indicate urgent treatment regardless of potassium level: peaked T waves, flattened P waves, prolonged PR interval, widened QRS 1, 2

Critical caveat: Exclude pseudo-hyperkalemia from hemolysis, repeated fist clenching, or poor phlebotomy technique before initiating aggressive treatment by repeating the measurement with proper technique or arterial sampling. 1, 2 However, never delay treatment while waiting for repeat labs if ECG changes are present—ECG changes indicate urgent need regardless of the exact potassium value. 2

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

For K+ ≥6.5 mEq/L OR any ECG changes:

• Calcium chloride (10%): 5-10 mL (500-1000 mg) IV over 2-5 minutes (preferred for rapid effect) 1, 2, 3
• Alternative: Calcium gluconate (10%): 15-30 mL IV over 2-5 minutes (use for peripheral IV access due to lower tissue injury risk) 1, 2

Key points about calcium:

• Effects begin within 1-3 minutes but last only 30-60 minutes 1, 2, 3
• Calcium does NOT lower serum potassium—it only stabilizes cardiac membranes temporarily 1, 2, 3
• Monitor ECG continuously during and for 5-10 minutes after administration 2
• If no ECG improvement within 5-10 minutes, repeat the dose 2
• Administer through central line when possible (calcium chloride causes severe tissue injury if extravasated) 1
• Never give calcium through the same IV line as sodium bicarbonate (precipitation occurs) 2

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

Administer all three agents together for maximum effect:

Insulin with Glucose (First-line)

• 10 units regular insulin IV with 25g glucose (50 mL of D50W) over 15-30 minutes 1, 2, 3
• Onset: 15-30 minutes; Duration: 4-6 hours 1, 2
• Monitor glucose every 2-4 hours to prevent hypoglycemia 1, 2
• Can be repeated every 4-6 hours if hyperkalemia persists, with careful glucose monitoring 2
• Higher risk of hypoglycemia in patients with low baseline glucose, no diabetes, female sex, and renal dysfunction 2

Nebulized Beta-2 Agonist (Adjunctive)

• Albuterol 10-20 mg nebulized over 15 minutes 1, 2, 3
• Onset: 15-30 minutes; Duration: 2-4 hours 1, 2
• Can reduce serum potassium by 0.5-1.0 mEq/L 1

Sodium Bicarbonate (ONLY if Metabolic Acidosis Present)

• 50 mEq IV over 5 minutes 1, 2
• Use ONLY in patients with concurrent metabolic acidosis (pH <7.35, bicarbonate <22 mEq/L) 1, 2
• Do not use without acidosis—it is ineffective and wastes time 2
• Onset: 30-60 minutes 2

Critical warning: These are temporizing measures only—rebound hyperkalemia can occur after 2 hours. 1 Failure to initiate concurrent potassium removal will result in recurrent life-threatening arrhythmias within 30-60 minutes. 2

Step 3: Eliminate Potassium from Body (Definitive Treatment)

For Patients with Adequate Renal Function:

• Loop diuretics: Furosemide 40-80 mg IV 1, 2, 3
• Increases renal potassium excretion 1, 2, 3
• Titrate to maintain euvolemia, not primarily for potassium management 2

Potassium Binders (Preferred for Subacute/Chronic Management):

Newer agents (preferred over sodium polystyrene sulfonate):

• Sodium zirconium cyclosilicate (SZC/Lokelma): 1, 2, 3

  • Acute: 10g three times daily for 48 hours
  • Maintenance: 5-15g once daily
  • Onset: ~1 hour (suitable for urgent scenarios)
  • Reduces potassium within 1 hour of single 10g dose

• Patiromer (Veltassa): 1, 2, 3

  • Starting dose: 8.4g once daily with food
  • Titrate up to 25.2g daily based on potassium levels
  • Onset: ~7 hours
  • Separate from other oral medications by at least 3 hours 2
  • Monitor magnesium levels (causes hypomagnesemia) 2

Avoid sodium polystyrene sulfonate (Kayexalate):

• Not efficacious for acute management 4
• Should not be used as emergency treatment due to delayed onset 5
• Associated with intestinal ischemia, colonic necrosis, and doubling of serious GI adverse events 2
• Reserved for subacute treatment only, if newer agents unavailable 1, 6

Hemodialysis:

• Most effective and reliable method for severe hyperkalemia 1, 2, 3, 7
• Indications: Severe hyperkalemia unresponsive to medical management, oliguria, end-stage renal disease 1, 2
• Monitor for rebound hyperkalemia 4-6 hours post-dialysis 2

Treatment Algorithm by Severity

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

1. Immediate: Calcium chloride 5-10 mL IV over 2-5 minutes 1, 2, 3
2. Within 15 minutes: Insulin 10 units + glucose 25g IV AND albuterol 10-20 mg nebulized 1, 2, 3
3. Concurrent: Loop diuretics OR hemodialysis (if renal failure) 1, 2, 3
4. Medication review: Temporarily discontinue/reduce RAAS inhibitors, NSAIDs, potassium-sparing diuretics 2

Moderate Hyperkalemia (K+ 6.0-6.4 mEq/L, No ECG Changes):

1. Insulin/glucose AND albuterol for intracellular shift 1, 3
2. Loop diuretics (if adequate renal function) 1, 2
3. Initiate potassium binder (patiromer or SZC) 1, 2
4. Review and adjust contributing medications 1, 2

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

1. Do NOT initiate acute interventions (calcium, insulin, albuterol) 2
2. Review and discontinue offending medications 1, 2, 3
3. Consider loop diuretics if adequate renal function 2
4. Initiate potassium binder for chronic management 1, 2, 3

Management of Patients on RAAS Inhibitors

Critical principle: For patients with cardiovascular disease or proteinuric CKD, do NOT permanently discontinue RAAS inhibitors—they provide mortality benefit and slow disease progression. 1, 2

For K+ 5.0-6.5 mEq/L:

• Initiate approved potassium-lowering agent (patiromer or SZC) 1, 2, 3
• Maintain RAAS inhibitor therapy unless alternative treatable cause identified 1, 2
• Monitor potassium closely 1, 2

For K+ >6.5 mEq/L:

• Temporarily discontinue or reduce RAAS inhibitor 1, 2
• Initiate potassium-lowering agent 1, 2
• Restart RAAS inhibitor at lower dose once K+ <5.0-5.5 mEq/L with concurrent potassium binder 2

Medications to Review and Adjust

Eliminate or reduce these contributing medications:

• ACE inhibitors, ARBs, mineralocorticoid receptor antagonists (MRAs) 1, 2
• NSAIDs (attenuate diuretic effects, impair renal potassium excretion) 2
• Potassium-sparing diuretics (amiloride, triamterene, spironolactone) 2
• Trimethoprim, heparin, beta-blockers 2
• Potassium supplements, salt substitutes (high potassium content) 2
• Never combine ACE inhibitor + ARB + MRA (excessive hyperkalemia risk) 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 severe initial hyperkalemia (>6.5 mEq/L): monitor every 2-4 hours initially 2
• High-risk patients (CKD, heart failure, diabetes, history of hyperkalemia) require more frequent monitoring 2
• Monitor magnesium levels in patients on patiromer (causes hypomagnesemia) 2

Common Pitfalls to Avoid

• Do not rely solely on ECG findings—they are highly variable and less sensitive than laboratory tests 2
• Never give insulin without glucose—hypoglycemia can be life-threatening 2
• Do not use sodium bicarbonate without metabolic acidosis—it is ineffective 2
• Remember that calcium, insulin, and beta-agonists do NOT remove potassium—they only temporize 2
• Do not delay calcium if ECG changes present while waiting for repeat potassium levels 2
• Avoid sodium polystyrene sulfonate in favor of newer potassium binders 2, 4