What are the initial laboratory evaluations and treatment options for a patient with hyperkalemia?

Initial Laboratory Evaluation and Treatment of Hyperkalemia

For a patient presenting with hyperkalemia, immediately obtain an ECG and serum potassium level, then initiate treatment based on severity: severe hyperkalemia (≥6.5 mEq/L) or any ECG changes require immediate IV calcium gluconate for cardiac membrane stabilization, followed by insulin/glucose and nebulized albuterol to shift potassium intracellularly. 1

Initial Laboratory Workup

Essential immediate tests include:

• Serum potassium level (verify it's not pseudohyperkalemia from hemolysis, repeated fist clenching, or poor phlebotomy technique—repeat with proper arterial sampling if suspected) 1
• 12-lead ECG to assess for peaked T waves, flattened P waves, prolonged PR interval, widened QRS complexes, or arrhythmias (these findings indicate urgent treatment regardless of exact potassium value) 1
• Complete metabolic panel including serum electrolytes (sodium, calcium, magnesium), blood urea nitrogen, serum creatinine, and glucose 2
• Complete blood count 2
• Urinalysis 2

Additional tests to identify etiology:

• Renal function assessment (eGFR calculation) to determine if impaired potassium excretion is contributing 1
• Medication review for RAAS inhibitors (ACE inhibitors, ARBs, mineralocorticoid antagonists), NSAIDs, potassium-sparing diuretics, trimethoprim, heparin, beta-blockers, and potassium supplements 1

Treatment Algorithm Based on Severity

Severe Hyperkalemia (K+ ≥6.5 mEq/L OR Any ECG Changes)

Immediate interventions (all given simultaneously):

1. Cardiac membrane stabilization (onset 1-3 minutes, duration 30-60 minutes):

   • Calcium gluconate 10%: 15-30 mL IV over 2-5 minutes 1
   • OR calcium chloride 10%: 5-10 mL IV over 2-5 minutes 1
   • Repeat dose if no ECG improvement within 5-10 minutes 1
   • Critical caveat: Calcium does NOT lower potassium—it only temporarily stabilizes cardiac membranes 1

2. Shift potassium intracellularly (onset 15-30 minutes, duration 4-6 hours):

   • Regular insulin 10 units IV + 25g dextrose (50 mL D50W) 1
   • Nebulized albuterol 10-20 mg in 4 mL 1
   • Monitor glucose closely to prevent hypoglycemia 1

3. Sodium bicarbonate (ONLY if concurrent metabolic acidosis present with pH <7.35, bicarbonate <22 mEq/L):

   • 50 mEq IV over 5 minutes 1
   • Do NOT use without metabolic acidosis—it is ineffective and wastes time 1

4. Remove potassium from body:

   • Loop diuretics (furosemide 40-80 mg IV) if adequate kidney function 1
   • Hemodialysis for severe cases unresponsive to medical management, oliguria, or end-stage renal disease 1
   • Initiate potassium binder (patiromer or sodium zirconium cyclosilicate) for sustained effect 1

Medication adjustments:

• Temporarily discontinue or reduce RAAS inhibitors 1
• Hold NSAIDs, potassium-sparing diuretics, trimethoprim, heparin, beta-blockers, potassium supplements, and salt substitutes 1

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

1. Shift potassium intracellularly:

   • Insulin 10 units IV + 25g dextrose 1
   • Nebulized albuterol 10-20 mg 1

2. Initiate potassium elimination:

   • Patiromer (Veltassa) 8.4 g once daily, titrated up to 25.2 g daily (onset ~7 hours) 1
   • OR sodium zirconium cyclosilicate (SZC/Lokelma) 10 g three times daily for 48 hours, then 5-15 g once daily (onset ~1 hour) 1
   • Loop diuretics if adequate renal function 1

3. Medication review and adjustment:

   • Reduce or temporarily hold RAAS inhibitors 1
   • Eliminate contributing medications 1

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

For patients on RAAS inhibitors with cardiovascular disease or proteinuric CKD:

• Initiate approved potassium-lowering agent (patiromer or SZC) while maintaining RAAS inhibitor therapy 1
• Do NOT permanently discontinue RAAS inhibitors—they provide mortality benefit 1

Treatment approach:

1. Dietary modification:

   • Limit high-potassium foods (processed foods, salt substitutes) 1
   • Avoid herbal supplements (alfalfa, dandelion, horsetail, nettle) 1

2. Medication optimization:

   • Review and eliminate NSAIDs, trimethoprim, heparin 1
   • Consider adding loop diuretics to increase urinary potassium excretion 1

3. Potassium binder therapy if recurrent or persistent:

   • Patiromer 8.4 g once daily 1
   • OR SZC 5-10 g once daily 1

Monitoring Protocol

Acute phase (during active treatment):

• Continuous cardiac monitoring if ECG changes present 1
• Recheck potassium every 2-4 hours until stabilized 1
• Monitor glucose closely after insulin administration 1

Post-acute phase:

• Recheck potassium within 1 week of starting or adjusting RAAS inhibitors 1
• Monitor at 1-2 weeks, 3 months, then every 6 months 1
• More frequent monitoring for high-risk patients (CKD, heart failure, diabetes) 1

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 1
• Never give insulin without glucose—hypoglycemia can be life-threatening 1
• Never use sodium bicarbonate without metabolic acidosis—it is ineffective without acidosis 1
• Remember calcium, insulin, and beta-agonists are temporizing measures only—they do NOT remove potassium from the body 1
• Do NOT rely solely on ECG findings—they are highly variable and less sensitive than laboratory tests 1
• Avoid sodium polystyrene sulfonate (Kayexalate) for acute management—it has delayed onset, limited efficacy, and risk of bowel necrosis 2, 1, 3