What are the steps for correcting hyperkalemia?

Hyperkalemia Correction: A Systematic Approach

For acute hyperkalemia with ECG changes or potassium ≥6.5 mEq/L, immediately administer IV calcium gluconate 15-30 mL (10% solution) over 2-5 minutes to stabilize cardiac membranes, followed by insulin 10 units IV with 25g dextrose and nebulized albuterol 20mg to shift potassium intracellularly. 1, 2, 3

Severity Classification and Initial Assessment

Classify hyperkalemia severity to guide treatment intensity:

• Mild: 5.0-5.9 mEq/L 1
• Moderate: 6.0-6.4 mEq/L 1
• Severe: ≥6.5 mEq/L 1

Before initiating treatment, verify this is true hyperkalemia and not pseudohyperkalemia from hemolysis, repeated fist clenching, or poor phlebotomy technique by repeating the measurement with proper arterial sampling. 1

Obtain an ECG immediately—the presence of peaked T waves, flattened P waves, prolonged PR interval, or widened QRS complexes indicates urgent treatment regardless of the potassium level. 1, 2, 3 However, ECG findings are highly variable and less sensitive than laboratory values, so do not rely solely on ECG to guide treatment decisions. 1

Acute Management Algorithm

Step 1: Cardiac Membrane Stabilization (Onset: 1-3 minutes)

If ECG changes are present, immediately give:

• IV calcium gluconate (10%): 15-30 mL over 2-5 minutes 1, 2
• Alternative: IV calcium chloride (10%): 5-10 mL over 2-5 minutes (use only with central access due to tissue injury risk) 1

Critical caveat: Calcium effects are temporary (30-60 minutes) and do not reduce total body potassium—this only buys time for definitive therapies. 1, 2 If no ECG improvement occurs within 5-10 minutes, repeat the calcium dose. 4, 1

Step 2: Intracellular Potassium Shift (Onset: 15-60 minutes)

Administer all of the following simultaneously for maximum effect:

• Insulin 10 units IV regular insulin with 25g dextrose (50 mL of D50W) 1, 3

  • Onset: 15-30 minutes, duration: 4-6 hours 1
  • Monitor glucose closely—check at 1-2 hours post-administration to prevent hypoglycemia 4, 1
  • Can be repeated every 4-6 hours if hyperkalemia persists 1

• Nebulized albuterol 20mg in 4 mL over 10-15 minutes 1, 5, 3

  • Onset: 30 minutes, duration: 2-4 hours 1
  • Highly effective and safe across all age groups 5

• Sodium bicarbonate 50-100 mEq IV ONLY if concurrent metabolic acidosis is present (pH <7.35, bicarbonate <22 mEq/L) 1

  • Onset: 30-60 minutes 1
  • Do not use in patients without acidosis—it is ineffective and potentially harmful 1

Recheck potassium levels 1-2 hours after initiating these therapies, then every 2-4 hours during the acute phase until stabilized. 4, 1

Step 3: Potassium Removal from the Body

For patients with adequate renal function:

• Furosemide 40-80 mg IV to increase urinary potassium excretion 1
• Consider saline diuresis if volume depleted 2, 3

For chronic or recurrent hyperkalemia:

• Sodium zirconium cyclosilicate (Lokelma): 10g three times daily for 48 hours, then 5-15g once daily for maintenance 1

  • Onset: ~1 hour, making it suitable for both acute and chronic management 1

• Patiromer (Veltassa): 8.4g once daily, titrated up to 25.2g daily based on potassium levels 1

  • Onset: ~7 hours, better for chronic management 1

Avoid sodium polystyrene sulfonate (Kayexalate)—it has delayed onset of action, limited efficacy data, and significant risk of bowel necrosis. 1, 6 The FDA label explicitly states it should not be used for emergency treatment of life-threatening hyperkalemia. 6

For severe hyperkalemia unresponsive to medical management, oliguria, or end-stage renal disease:

• Hemodialysis is the most reliable and effective method for potassium removal 1, 2, 3

Chronic Hyperkalemia Management

Medication Review and Adjustment

Identify and address contributing medications:

• NSAIDs, trimethoprim, heparin, beta-blockers, potassium supplements, salt substitutes 1
• Do NOT routinely discontinue RAAS inhibitors (ACE inhibitors, ARBs, mineralocorticoid antagonists)—these provide critical mortality benefit in cardiovascular and renal disease 1

For patients on RAAS inhibitors with potassium 5.0-6.5 mEq/L:

• Initiate patiromer or sodium zirconium cyclosilicate while maintaining RAAS inhibitor therapy 1
• This approach allows continuation of life-saving medications while controlling potassium 7, 1

For patients with potassium >6.5 mEq/L:

• Temporarily discontinue or reduce RAAS inhibitor dose 1
• Initiate potassium-lowering agent immediately 1
• Restart RAAS inhibitor at lower dose once potassium <5.0 mEq/L with concurrent potassium binder therapy 1

Dietary Considerations

Contrary to traditional teaching, evidence linking dietary potassium intake to serum levels is limited, and a potassium-rich diet provides cardiovascular benefits including blood pressure reduction. 1 However, for patients with recurrent hyperkalemia:

• Limit processed foods rich in bioavailable potassium 4
• Avoid salt substitutes containing potassium 4
• Avoid herbal supplements that raise potassium (alfalfa, dandelion, horsetail, nettle) 4

Monitoring Protocol

For patients starting or escalating RAAS inhibitors:

• Check potassium and renal function within 7-10 days 1
• Reassess at 1-2 weeks, 3 months, then every 6 months 4

For patients on potassium binders:

• Check potassium within 1 week of initiation 1
• Monitor weekly during dose titration 1
• Critical: Monitor closely not only for efficacy but also to protect against hypokalemia, which may be even more dangerous than hyperkalemia 4

Increase monitoring frequency for high-risk patients:

• Chronic kidney disease (especially eGFR <45 mL/min) 7, 1
• Heart failure 7, 1
• Diabetes mellitus 7, 1
• History of recurrent hyperkalemia 7, 1

Special Population: CKD Patients

Patients with advanced CKD tolerate higher potassium levels due to compensatory mechanisms—the optimal range is broader (3.3-5.5 mEq/L for stage 4-5 CKD versus 3.5-5.0 mEq/L for stage 1-2 CKD). 7, 1 However, maintaining target potassium 4.0-5.0 mEq/L still minimizes mortality risk. 1

Aggressively maintain RAAS inhibitors in proteinuric CKD using potassium binders, as these drugs slow CKD progression and improve cardiovascular outcomes. 1

Critical Pitfalls to Avoid

• Never rely solely on ECG findings—they are highly variable and less sensitive than laboratory tests 1
• Never use sodium bicarbonate without concurrent metabolic acidosis—it is only indicated when acidosis is present 1
• Always administer glucose with insulin to prevent hypoglycemia 1, 3
• Remember that calcium, insulin, and beta-agonists only temporize—they do not remove potassium from the body 1, 2
• Do not permanently discontinue RAAS inhibitors—use potassium binders to enable continuation of these life-saving medications 1
• Verify adequate urine output before administering potassium-containing IV fluids 4