What medications can be used to lower potassium levels in a patient with hyperkalemia?

Medications to Lower Potassium Levels in Hyperkalemia

For acute severe hyperkalemia (>6.5 mEq/L or with ECG changes), immediately administer IV calcium gluconate for cardiac membrane stabilization, followed by insulin with glucose and nebulized albuterol to shift potassium intracellularly, then initiate potassium removal with newer potassium binders (patiromer or sodium zirconium cyclosilicate) or hemodialysis for definitive treatment. 1, 2

Acute Emergency Management (Severe Hyperkalemia >6.5 mEq/L or ECG Changes)

Immediate Cardiac Membrane Stabilization

• Administer IV calcium gluconate 15-30 mL of 10% solution over 2-5 minutes (or calcium chloride 5-10 mL of 10% solution) as first-line therapy when ECG changes are present 1, 2
• Onset of cardioprotective effects occurs within 1-3 minutes, but duration is only 30-60 minutes 1, 2
• Critical caveat: Calcium does NOT lower serum potassium—it only temporarily stabilizes cardiac membranes 1, 2
• If no ECG improvement within 5-10 minutes, repeat the dose 2
• Continuous cardiac monitoring is mandatory during and after administration 2

Intracellular Potassium Shift (Does Not Remove Potassium from Body)

• Insulin 10 units regular IV plus 25 grams dextrose (50 mL of 50% dextrose) redistributes potassium within 30-60 minutes with effects lasting 4-6 hours 1, 2, 3
• Nebulized albuterol 10-20 mg in 4 mL as adjunctive therapy, with onset within 30 minutes and duration of 2-4 hours 1, 2
• Sodium bicarbonate 50 mEq IV over 5 minutes ONLY if concurrent metabolic acidosis is present (pH <7.35, bicarbonate <22 mEq/L) 1, 2
• Never use sodium bicarbonate without metabolic acidosis—it is ineffective and wastes time 2
• Ensure glucose is administered with insulin to prevent life-threatening hypoglycemia 2

Definitive Potassium Removal from Body

• Loop diuretics (furosemide 40-80 mg IV) increase renal potassium excretion in patients with adequate kidney function (eGFR >30 mL/min) 1, 2
• Hemodialysis is the most effective and reliable method for severe hyperkalemia, especially in patients with renal failure, oliguria, or hyperkalemia unresponsive to medical management 1, 2, 4

Chronic/Recurrent Hyperkalemia Management

Newer Potassium Binders (First-Line for Long-Term Management)

Sodium Zirconium Cyclosilicate (SZC/Lokelma) 1, 2, 5

• Dosing: 10 g three times daily for 48 hours, then 5-15 g once daily for maintenance 1, 2
• Onset of action: ~1 hour, making it suitable for urgent outpatient scenarios 1, 2
• In clinical trials (Study 1), 10 g TID reduced mean serum potassium by -0.7 mEq/L at 48 hours in patients with baseline potassium 5.3 mEq/L 5
• Patients with higher starting potassium levels (>5.5 mEq/L) had greater response: mean reduction of -1.1 mEq/L at 48 hours 5
• Effective in patients with chronic kidney disease, heart failure, diabetes mellitus, and those on RAAS inhibitor therapy 5
• Mechanism: Exchanges hydrogen and sodium for potassium in the GI tract 2, 6

Patiromer (Veltassa) 1, 2

• Dosing: Start 8.4 g once daily with food, titrate up to 25.2 g daily based on potassium response 1, 2
• Onset of action: ~7 hours 1, 2
• Must be separated from other oral medications by at least 3 hours to avoid reduced absorption 2
• Mechanism: Binds potassium in exchange for calcium in the colon, increasing fecal excretion 1, 2
• Monitor magnesium levels as patiromer causes hypomagnesemia 2

Older Potassium Binders (Avoid in Most Cases)

Sodium Polystyrene Sulfonate (SPS/Kayexalate) 1, 2

• Should be avoided due to serious safety concerns: intestinal ischemia, colonic necrosis, and doubling of risk for serious GI adverse events 1, 2
• Delayed onset of action, variable efficacy, and lack of quality evidence supporting its use 1, 2
• Reserved only for subacute treatment when newer agents are unavailable 3, 4

Medication Management Strategy

Maintain Life-Saving RAAS Inhibitors

• Do NOT permanently discontinue ACE inhibitors, ARBs, or mineralocorticoid receptor antagonists in patients with cardiovascular disease, heart failure, or proteinuric CKD 1, 2
• These medications provide mortality benefit and slow disease progression 1, 2
• For potassium 5.0-6.5 mEq/L: Initiate patiromer or SZC while maintaining RAAS inhibitor therapy 1, 2
• For potassium >6.5 mEq/L: Temporarily reduce or hold RAAS inhibitor, initiate potassium binder, then restart at lower dose once potassium <5.0 mEq/L 1, 2

Eliminate Contributing Medications

• Discontinue or reduce: NSAIDs, potassium-sparing diuretics (spironolactone, amiloride, triamterene), trimethoprim, heparin, beta-blockers, potassium supplements, and salt substitutes 1, 2
• Avoid triple combination of ACE inhibitor + ARB + mineralocorticoid antagonist due to excessive hyperkalemia risk 2

Monitoring Protocol

• Check potassium within 1 week of starting or escalating RAAS inhibitors 1, 2
• Reassess 7-10 days after initiating potassium binder therapy 1, 2
• For high-risk patients (CKD, diabetes, heart failure, history of hyperkalemia), individualize monitoring frequency with more frequent checks 1, 2
• Monitor closely for hypokalemia when using potassium binders, as hypokalemia may be even more dangerous than hyperkalemia 7

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 rely on calcium, insulin, or beta-agonists alone—these are temporizing measures that do NOT remove potassium from the body 1, 2
• Never give insulin without glucose—hypoglycemia can be life-threatening 2
• Never use sodium bicarbonate without metabolic acidosis—it is ineffective in patients without acidosis 1, 2
• Never permanently discontinue beneficial RAAS inhibitors—use dose reduction plus potassium binders instead 1, 2