What is the emergent treatment protocol for severe hyperkalemia in an adult patient?

Emergent Treatment of Severe Hyperkalemia

For severe hyperkalemia (≥6.5 mEq/L) or any ECG changes, immediately administer IV calcium gluconate to stabilize the cardiac membrane, followed simultaneously by insulin-glucose and nebulized albuterol to shift potassium intracellularly, then initiate definitive potassium removal with hemodialysis or loop diuretics depending on renal function. 1, 2

Immediate Cardiac Membrane Stabilization (Within 1-3 Minutes)

Administer IV calcium first—this is your only immediate protection against fatal arrhythmias. 1, 2

• Give calcium gluconate 10%: 15-30 mL IV over 2-5 minutes (preferred for peripheral access) 1, 2
• Alternative: calcium chloride 10%: 5-10 mL IV over 2-5 minutes if central access available (more potent) 1
• Onset of action: 1-3 minutes, but effect lasts only 30-60 minutes 1, 2
• Critical caveat: Calcium does NOT lower potassium—it only temporarily protects the heart 1, 2
• Repeat the dose in 5-10 minutes if ECG changes persist 1

When to Give Calcium

• Serum potassium >6.5 mEq/L regardless of ECG 1, 2
• Any ECG changes: peaked T waves, flattened P waves, prolonged PR interval, widened QRS, or arrhythmias 1, 2
• Do not delay calcium while waiting for repeat labs if ECG changes are present 1, 2

Intracellular Potassium Shift (Administer Simultaneously—Within 15-30 Minutes)

Give all three agents together for maximum effect: 1

Insulin-Glucose (Most Reliable)

• Insulin regular 10 units IV push + dextrose 50% (D50W) 50 mL (25 grams) 1, 2
• Lowers potassium by 0.5-1.2 mEq/L within 30-60 minutes 1
• Duration: 4-6 hours 1
• Never give insulin without glucose—hypoglycemia can be fatal 1, 2

Nebulized Albuterol (Synergistic Effect)

• Albuterol 10-20 mg in 4 mL nebulized over 10-15 minutes 1, 2
• Lowers potassium by 0.5-1.0 mEq/L within 30 minutes 1
• Duration: 2-4 hours 1
• Can be repeated every 2 hours if needed 1
• Combined with insulin produces greater reduction than either alone 1

Sodium Bicarbonate (ONLY with Metabolic Acidosis)

• Give 50 mEq IV over 5 minutes ONLY if pH <7.35 and bicarbonate <22 mEq/L 1, 2
• Onset: 30-60 minutes 1
• Do not use without documented acidosis—it is ineffective and wastes time 1, 2

Definitive Potassium Removal (Within Hours)

Hemodialysis (Most Reliable Method)

Hemodialysis is the gold standard for severe hyperkalemia. 1, 3

Absolute indications: 1

• Serum potassium >6.5 mEq/L unresponsive to medical therapy
• Oliguria or anuria
• End-stage renal disease
• Ongoing potassium release (tumor lysis syndrome, rhabdomyolysis)
• Severe renal impairment (eGFR <15 mL/min)
• Persistent ECG changes despite medical management

In hemodynamically unstable patients, use continuous renal replacement therapy (CRRT) instead of intermittent hemodialysis to minimize rapid fluid shifts. 1

Loop Diuretics (If Adequate Renal Function)

• Furosemide 40-80 mg IV to increase renal potassium excretion 1, 2
• Only effective when eGFR >30 mL/min and patient is non-oliguric 1
• Titrate to maintain euvolemia, not primarily for potassium management 1

Potassium Binders (Sub-Acute Management)

Sodium polystyrene sulfonate (Kayexalate) should be avoided due to risk of bowel necrosis and limited efficacy. 1, 2

Preferred agents: 1, 2

• Sodium zirconium cyclosilicate (SZC/Lokelma): 10 g three times daily for 48 hours, then 5-15 g once daily
  • Onset: ~1 hour (suitable for urgent scenarios)
• Patiromer (Veltassa): 8.4 g once daily with food, titrated up to 25.2 g daily
  • Onset: ~7 hours (for sub-acute/chronic control)
  • Must be separated from other oral meds by ≥3 hours

Medication Management During Acute Episode

Hold immediately when potassium >6.5 mEq/L: 1, 2

• RAAS inhibitors (ACE inhibitors, ARBs, mineralocorticoid receptor antagonists)
• NSAIDs
• Potassium-sparing diuretics
• Trimethoprim-containing agents
• Heparin
• Beta-blockers
• Potassium supplements and salt substitutes

After acute resolution: 1

• Restart RAAS inhibitors at lower dose once potassium <5.0 mEq/L (they provide mortality benefit in cardiovascular and renal disease)
• Initiate potassium binder (SZC or patiromer) to enable continuation of life-saving RAAS therapy

Monitoring Protocol

Acute Phase

• Re-measure potassium 1-2 hours after insulin/glucose or beta-agonist therapy 1
• Continue checks every 2-4 hours until stable 1
• Obtain repeat ECG to confirm resolution of cardiac changes 1

Post-Acute Phase

• Check potassium within 1 week after initiating or escalating RAAS inhibitors 1, 2
• Reassess 7-10 days after starting potassium binder 1, 2
• Individualize monitoring frequency based on renal function, heart failure, diabetes, or prior hyperkalemia 1, 2

Critical Pitfalls to Avoid

• Do not delay calcium administration while awaiting repeat potassium levels when ECG changes are present 1, 2
• Never give insulin without glucose—hypoglycemia can be fatal 1, 2
• Recognize that calcium, insulin, and beta-agonists are temporizing measures only—they do NOT remove potassium from the body 1, 2
• Do not use sodium bicarbonate without documented metabolic acidosis (pH <7.35, bicarbonate <22 mEq/L) 1, 2
• Do not permanently discontinue RAAS inhibitors—use potassium binders to maintain these life-saving medications 1, 2
• Do not rely solely on ECG findings—they are highly variable and less sensitive than laboratory tests 1, 2

Special Populations

Patients with Cardiovascular Disease

• Maintain RAAS inhibitors using potassium binders rather than discontinuing these medications 1, 2
• Discontinuing RAAS inhibitors leads to worse cardiovascular and renal outcomes 1

Patients with Chronic Kidney Disease

• Maintain RAAS inhibitors aggressively in proteinuric CKD using potassium binders—these drugs slow CKD progression 1
• Optimal potassium range is broader in advanced CKD: 3.3-5.5 mEq/L for stage 4-5 CKD 1

Hemodynamically Unstable Patients

• Prefer CRRT over intermittent hemodialysis to minimize rapid fluid shifts and reduce intradialytic hypotension risk 1