What are all the potassium-lowering medications and therapies for a patient with hyperkalemia?

Potassium-Lowering Medications and Therapies for Hyperkalemia

For acute, life-threatening hyperkalemia, use IV calcium gluconate for cardiac membrane stabilization, followed by insulin/glucose and nebulized albuterol to shift potassium intracellularly, then hemodialysis or potassium binders to remove potassium from the body. 1

Acute Hyperkalemia Management: Temporizing Agents (Do NOT Remove Potassium)

Calcium (Cardiac Membrane Stabilization)

• Calcium gluconate 10%: 15-30 mL IV over 2-5 minutes or calcium chloride 10%: 5-10 mL IV over 2-5 minutes provides immediate cardiac protection within 1-3 minutes 1
• Effects last only 30-60 minutes and do NOT lower serum potassium—this is purely a temporizing measure to prevent arrhythmias 1, 2
• Repeat dosing may be necessary if no ECG improvement within 5-10 minutes 1
• Critical caveat: In malignant hyperthermia with hyperkalemia, calcium should only be used in extremis as it may contribute to myoplasmic calcium overload 1

Insulin/Glucose (Intracellular Shift)

• Standard dose: 10 units regular insulin IV with 25g dextrose (50 mL of D50W) 1
• Alternative dosing: 0.1 units/kg (approximately 5-7 units in adults) 1
• Onset within 15-30 minutes, effects last 4-6 hours 1, 2
• Can be repeated every 4-6 hours if hyperkalemia persists, with careful glucose and potassium monitoring 1
• Never give insulin if potassium <3.3 mEq/L 1
• High-risk populations for hypoglycemia: low baseline glucose, no diabetes history, female sex, altered renal function 1

Beta-2 Agonists (Intracellular Shift)

• Nebulized albuterol 10-20 mg in 4 mL as adjunctive therapy 1, 2
• Onset within 15-30 minutes, effects last 2-4 hours 1
• Less effective as monotherapy but synergistic with insulin 1

Sodium Bicarbonate (Intracellular Shift—ONLY with Metabolic Acidosis)

• 50 mEq IV over 5 minutes ONLY if concurrent metabolic acidosis present (pH <7.35, bicarbonate <22 mEq/L) 1, 2
• Mechanism: promotes potassium excretion through increased distal sodium delivery and counters acidosis-induced potassium release 1
• Effects take 30-60 minutes to manifest 1, 2
• Do NOT use without metabolic acidosis—it is ineffective and wastes time 1

Acute Hyperkalemia Management: Potassium Removal Agents

Loop Diuretics (Renal Excretion)

• Furosemide 40-80 mg IV increases renal potassium excretion in patients with adequate kidney function 1, 2
• Only effective if eGFR >30 mL/min 1
• Should be titrated to maintain euvolemia, not primarily for potassium management 1

Hemodialysis (Definitive Removal)

• Most effective and reliable method for severe hyperkalemia, especially in renal failure 1, 2
• Reserved for severe cases unresponsive to medical management, oliguria, or end-stage renal disease 1
• Potassium levels can rebound 4-6 hours post-dialysis as intracellular potassium redistributes 1

Chronic Hyperkalemia Management: Potassium Binders

Patiromer (Veltassa)

• Starting dose: 8.4 g once daily with food for K+ 5.0-5.5 mEq/L 1, 3
• Titrate up to 16.8 g or 25.2 g daily based on potassium response 1, 3
• Onset of action: ~7 hours 1
• Mechanism: binds potassium in exchange for calcium in the colon, increasing fecal excretion 1
• Must be separated from other oral medications by at least 3 hours (before or after) to avoid reduced absorption 1, 3
• Monitor magnesium levels—causes hypomagnesemia 1
• FDA-approved for adults and pediatric patients ≥12 years 3

Sodium Zirconium Cyclosilicate (SZC/Lokelma)

• Initial dosing: 10 g three times daily for 48 hours, then 5-15 g once daily for maintenance 1, 2
• Onset of action: ~1 hour—suitable for more urgent outpatient scenarios 1, 2
• Mechanism: highly selective potassium binding, exchanging hydrogen and sodium for potassium 1
• May improve metabolic acidosis by increasing ammonium excretion 1
• Monitor for edema due to sodium content 1

Sodium Polystyrene Sulfonate (Kayexalate)—AVOID

• Significant limitations: delayed onset, risk of bowel necrosis, and lack of efficacy data 1, 2
• Associated with intestinal ischemia, colonic necrosis, and doubling of serious GI adverse events 1
• Should be avoided for acute management and chronic use 1, 2

Additional Chronic Management Strategies

Dietary Modification

• Limit foods rich in bioavailable potassium, especially processed foods 1
• Avoid salt substitutes containing potassium 1, 2
• Avoid herbal supplements that raise K+: alfalfa, dandelion, horsetail, nettle 1
• Evidence linking dietary potassium to serum levels is limited—potassium-rich diets provide cardiovascular benefits 1

Medication Adjustments

• Review and adjust contributing medications: NSAIDs, trimethoprim, heparin, beta-blockers, potassium supplements 1, 2
• Maintain RAAS inhibitors (ACE inhibitors, ARBs, MRAs) whenever possible using potassium binders rather than discontinuing these life-saving medications 1, 2
• For K+ 5.0-6.5 mEq/L on RAAS inhibitors: initiate potassium binder and maintain RAAS therapy 1, 2
• For K+ >6.5 mEq/L: temporarily discontinue or reduce RAAS inhibitor, initiate potassium binder 1, 2

Fludrocortisone (Use Cautiously)

• Increases potassium excretion but carries risks of fluid retention, hypertension, and vascular injury 1
• Should be used cautiously and only when other options are exhausted 1

Monitoring Protocol

Acute Hyperkalemia

• Recheck potassium within 1-2 hours after IV potassium correction (insulin/glucose, beta-agonists) 1
• Continue monitoring every 2-4 hours during acute treatment phase until stabilized 1
• If no ECG improvement within 5-10 minutes after calcium, give second dose 1

Chronic Hyperkalemia

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

Critical Pitfalls to Avoid

• Never delay treatment while waiting for repeat lab confirmation if ECG changes are present 1
• Never use sodium bicarbonate without metabolic acidosis—it is ineffective 1, 2
• Never give insulin without glucose—hypoglycemia can be life-threatening 1
• Remember that calcium, insulin, and beta-agonists do NOT remove potassium from the body—they only temporize 1
• Do not rely solely on ECG findings—they are highly variable and less sensitive than laboratory tests 1
• Do not permanently discontinue RAAS inhibitors in cardiovascular disease or proteinuric CKD—use potassium binders instead 1, 2