What are the treatment options for a patient with hyperkalemia?

Treatment of Hyperkalemia

For acute hyperkalemia, immediately stabilize the cardiac membrane with IV calcium, shift potassium intracellularly with insulin/glucose and albuterol, then eliminate potassium from the body using diuretics, newer potassium binders, or hemodialysis—never use sodium polystyrene sulfonate for acute management due to delayed onset and serious safety concerns. 1, 2

Severity Classification

Assess severity and ECG changes first to determine urgency:

• 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, which is 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

Exclude pseudo-hyperkalemia from hemolysis or improper sampling before initiating aggressive treatment by repeating measurement with appropriate technique or arterial sampling. 1, 2

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

Administer IV calcium first if potassium >6.5 mEq/L OR any ECG changes are present:

• Calcium chloride (10%): 5-10 mL (500-1000 mg) IV over 2-5 minutes (preferred, provides more rapid increase in ionized calcium) 1, 2
• Calcium gluconate (10%): 15-30 mL IV over 2-5 minutes (alternative, safer for peripheral IV) 1, 2
• Onset: 1-3 minutes, duration: 30-60 minutes (temporary only) 1, 2
• Calcium does NOT lower serum potassium—it only stabilizes cardiac membranes temporarily 1, 2

Administration considerations:

• Calcium chloride should be given through central venous catheter when possible, as extravasation through peripheral IV may cause severe skin and soft tissue injury 1
• Monitor heart rate during administration and stop if symptomatic bradycardia occurs 1
• If no ECG improvement within 5-10 minutes, repeat the dose 1, 2
• Never administer calcium through the same IV line as sodium bicarbonate (precipitation will occur) 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: 10 units regular insulin IV + 25g glucose (50 mL of D50W) over 15-30 minutes 1, 2

  • Onset: 15-30 minutes, duration: 4-6 hours 1, 2
  • Can be repeated every 4-6 hours if hyperkalemia persists, with careful monitoring of glucose and potassium every 2-4 hours 1, 2
  • Always verify glucose is administered with insulin to prevent hypoglycemia 2
  • Patients with low baseline glucose, no diabetes, female sex, and altered renal function are at higher risk of hypoglycemia 1

• Nebulized albuterol: 10-20 mg over 15 minutes 1, 2

  • Onset: 15-30 minutes, duration: 2-4 hours 1, 2
  • Can reduce serum potassium by approximately 0.5-1.0 mEq/L 1

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

  • Most effective in patients with concurrent metabolic acidosis 1, 2
  • Effects take 30-60 minutes to manifest 1, 2
  • Do not use without metabolic acidosis—it is ineffective and wastes time 2

Critical warning: These are temporizing measures only—they do NOT remove potassium from the body, and rebound hyperkalemia can occur after 2 hours. 1, 2

Step 3: Eliminate Potassium from Body (Definitive Treatment)

Choose method based on renal function and clinical context:

• Loop diuretics (furosemide 40-80 mg IV): Effective only in patients with adequate renal function (eGFR >30 mL/min) 1, 2

  • Increases renal potassium excretion by stimulating flow to renal collecting ducts 1, 2
  • Should be titrated to maintain euvolemia, not primarily for potassium management 2

• Newer 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
    • Onset: ~1 hour (suitable for more urgent scenarios) 1, 2
    • Reduces serum potassium within 1 hour of a single 10g dose 2
  • Patiromer (Veltassa): 8.4g once daily with food, titrated up to 25.2g daily based on potassium levels 1, 2
    • Onset: ~7 hours 2
    • Must be separated from other oral medications by at least 3 hours 1, 2
    • Binds potassium in exchange for calcium in the colon 2

• Avoid sodium polystyrene sulfonate (Kayexalate): Delayed onset of action, limited efficacy, and risk of bowel necrosis and intestinal ischemia 1, 2, 3, 4

  • FDA label states it should not be used as emergency treatment for life-threatening hyperkalemia due to delayed onset of action 3, 4

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

  • Potassium levels can rebound as intracellular potassium redistributes to extracellular space 2
  • Monitor patients with severe initial hyperkalemia (>6.5 mEq/L) every 2-4 hours initially due to rebound risk 2

Chronic Hyperkalemia Management

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

• Potassium 5.0-6.5 mEq/L: Initiate approved potassium-lowering agent (patiromer or SZC) and maintain RAAS inhibitor therapy unless alternative treatable cause identified 1, 2

  • Do not permanently discontinue RAAS inhibitors—they provide mortality benefit in cardiovascular and renal disease 1, 2

• Potassium >6.5 mEq/L: Discontinue or reduce RAAS inhibitor temporarily, initiate potassium-lowering agent when levels >5.0 mEq/L, monitor closely 1, 2

  • Restart RAAS inhibitor at lower dose once potassium <5.5 mEq/L with concurrent potassium binder therapy 2

Review and adjust contributing medications:

• ACE inhibitors, ARBs, mineralocorticoid receptor antagonists 1, 2
• NSAIDs (cause sodium retention, worsen renal function, increase hyperkalemia risk) 1, 2
• Potassium-sparing diuretics (spironolactone, amiloride, triamterene) 2
• Beta-blockers 1, 2
• Trimethoprim, heparin 2
• Potassium supplements and salt substitutes 1, 2

Dietary considerations:

• Limit foods rich in bioavailable potassium, especially processed foods 2
• Avoid salt substitutes containing potassium 2
• Avoid herbal supplements that raise K+ (alfalfa, dandelion, horsetail, nettle) 2
• Evidence linking dietary potassium intake to serum levels is limited—potassium-rich diets provide cardiovascular benefits including blood pressure reduction 2

Monitoring Protocol

Acute phase:

• Check potassium every 2-4 hours during acute treatment until stabilized 1, 2
• Obtain ECG if initial presentation included cardiac changes to document resolution 2

Chronic management:

• Check potassium within 1 week of starting or escalating RAAS inhibitors 1, 2
• Reassess 7-10 days after initiating potassium binder therapy 2
• Individualize monitoring frequency based on eGFR, heart failure, diabetes, or history of hyperkalemia 2
• High-risk patients (CKD, diabetes, heart failure) require more frequent monitoring 1, 2

Critical Pitfalls to Avoid

• Never delay treatment while waiting for repeat lab confirmation if ECG changes are present—ECG changes indicate urgent need regardless of exact potassium value 2
• Never use sodium bicarbonate without metabolic acidosis—it is ineffective 2
• Never give insulin without glucose—hypoglycemia can be life-threatening 2
• Remember calcium, insulin, and beta-agonists do NOT remove potassium from the body—they only temporize 1, 2
• Do not rely solely on ECG findings—they are highly variable and less sensitive than laboratory tests 2
• Avoid sodium polystyrene sulfonate for acute management—delayed onset and serious GI adverse effects 1, 2, 3, 4

Special Populations

CKD patients:

• Patients with advanced CKD tolerate higher potassium levels (3.3-5.5 mEq/L for stage 4-5 CKD) due to compensatory mechanisms 2
• Maintain RAAS inhibitors aggressively using potassium binders, as these drugs slow CKD progression 1, 2
• Dialysis reserved for severe cases unresponsive to medical management, oliguria, or ESRD 2

Heart failure patients:

• Both hypokalemia and hyperkalemia increase mortality risk—target 4.0-5.0 mEq/L 2
• Use potassium binders to enable continuation of life-saving RAAS inhibitor therapy 1, 2