Hyperkalemia Management Protocol

Immediate Assessment and Classification

Verify true hyperkalemia by excluding pseudohyperkalemia from hemolysis, repeated fist clenching, or poor phlebotomy technique—repeat with proper arterial sampling if uncertain. 1, 2

Severity Classification:

Mild: 5.0-5.9 mEq/L 1, 2
Moderate: 6.0-6.4 mEq/L 1, 2
Severe: ≥6.5 mEq/L 1, 2

Obtain immediate ECG regardless of potassium level—ECG changes (peaked T waves, flattened P waves, prolonged PR interval, widened QRS) mandate urgent treatment even if potassium appears only mildly elevated. 1, 2 However, do not rely solely on ECG findings as they are highly variable and less sensitive than laboratory values. 1

Acute Hyperkalemia Management (Emergency Treatment)

Step 1: Cardiac Membrane Stabilization (Within 1-3 Minutes)

Administer IV calcium immediately if potassium >6.5 mEq/L OR any ECG changes are present: 1, 2

Calcium gluconate (10%): 15-30 mL IV over 2-5 minutes 3, 1
OR Calcium chloride (10%): 5-10 mL IV over 2-5 minutes (use central line if available due to tissue injury risk) 1

Critical caveat: Calcium does NOT lower potassium—it only stabilizes cardiac membranes temporarily for 30-60 minutes. 3, 1 If no ECG improvement within 5-10 minutes, repeat the dose. 3

Step 2: Shift Potassium Intracellularly (Within 15-30 Minutes)

Administer all three agents together for maximum effect: 1

Insulin + Glucose: 10 units regular insulin IV with 25g dextrose (50 mL of 50% dextrose or 250 mL of 10% dextrose) 1, 2
- Onset: 15-30 minutes, Duration: 4-6 hours 1
- Never give insulin without glucose—hypoglycemia can be life-threatening 1
- Monitor glucose every 2-4 hours after administration 1
- Can repeat every 4-6 hours if hyperkalemia persists 1
Nebulized Albuterol: 10-20 mg in 4 mL nebulized over 10 minutes 1, 2
- Onset: 15-30 minutes, Duration: 2-4 hours 1
- Use as adjunctive therapy to insulin/glucose 1
Sodium Bicarbonate: 50 mEq IV over 5 minutes ONLY if concurrent metabolic acidosis present (pH <7.35, bicarbonate <22 mEq/L) 3, 1
- Onset: 30-60 minutes 1
- Do not use without metabolic acidosis—it is ineffective and wastes time 1

Step 3: Remove Potassium from Body (Definitive Treatment)

Loop Diuretics (if adequate renal function):

Furosemide 40-80 mg IV to increase urinary potassium excretion 1
Requires eGFR sufficient for diuretic response 1

Hemodialysis:

Most effective and reliable method for severe hyperkalemia, especially in renal failure, oliguria, or cases unresponsive to medical management 1, 4
Use as adjunctive therapy after instituting other approaches 3

Potassium Binders (for subacute/chronic management—NOT emergency):

Sodium polystyrene sulfonate (SPS/Kayexalate): Delayed onset, risk of bowel necrosis—avoid for acute management 1, 5
Newer agents preferred (see chronic management below) 1

Step 4: Medication Review During Acute Episode

Temporarily discontinue or reduce at K+ ≥6.5 mEq/L: 1

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

Chronic Hyperkalemia Management

Primary Goal: Maintain Life-Saving RAAS Inhibitors

Do NOT permanently discontinue RAAS inhibitors—they provide mortality benefit in cardiovascular and renal disease. 1 Use potassium binders to enable continuation of these medications. 1

Treatment Algorithm Based on Potassium Level

Potassium 5.0-6.5 mEq/L on RAAS inhibitors:

Initiate approved potassium-lowering agent (patiromer or SZC) while maintaining RAAS inhibitor therapy 1
Eliminate contributing medications: NSAIDs, trimethoprim, heparin, potassium supplements, salt substitutes 1
Optimize diuretic therapy if adequate renal function present 1

Potassium >6.5 mEq/L on RAAS inhibitors:

Temporarily discontinue or reduce RAAS inhibitor 1
Initiate potassium binder immediately 1
Restart RAAS inhibitor at lower dose once K+ <5.5 mEq/L 1

Preferred Potassium Binders

Patiromer (Veltassa): 1

Starting dose: 8.4g once daily
Titrate up to 25.2g daily based on potassium levels
Onset: ~7 hours
Take separately from other medications (3 hours before or after)

Sodium Zirconium Cyclosilicate (SZC/Lokelma): 1

Acute phase: 10g three times daily for 48 hours
Maintenance: 5-15g once daily
Onset: ~1 hour (fastest-acting binder)
Can be used for both acute (≥5.8 mEq/L) and chronic management

Avoid Sodium Polystyrene Sulfonate (Kayexalate): Delayed onset, risk of bowel necrosis, significant limitations. 1, 5

Additional Chronic Management Strategies

Loop or Thiazide Diuretics:

Promote urinary potassium excretion by stimulating flow to renal collecting ducts 3, 1
Furosemide 40-80 mg daily if adequate renal function 1
Titrate to maintain euvolemia, not primarily for potassium management 1

Fludrocortisone:

Increases potassium excretion but carries risks of fluid retention, hypertension, vascular injury 3, 1
Use cautiously and only when other options exhausted 3

Monitoring Protocol

Initial monitoring when starting/escalating RAAS inhibitors:

Check potassium within 1 week of starting or dose escalation 1, 2
Reassess 7-10 days after dose changes 1, 2

Ongoing monitoring frequency (individualized based on risk):

High-risk patients (CKD, heart failure, diabetes, history of hyperkalemia): More frequent monitoring 1, 2
CKD Stage 4-5: Target potassium 3.3-5.5 mEq/L (broader range tolerated) 1
CKD Stage 1-2: Target potassium 3.5-5.0 mEq/L 1
Optimal target for mortality reduction: 4.0-5.0 mEq/L 1

After initiating potassium binder:

Reassess at 1-2 weeks, 3 months, then every 6 months 1
Monitor closely for hypokalemia—may be more dangerous than hyperkalemia 1

Special Population Considerations

Patients with CKD

Maintain RAAS inhibitors aggressively in proteinuric CKD using potassium binders—these drugs slow CKD progression and provide mortality benefit. 1

For moderate hyperkalemia (6.0-6.4 mEq/L) with no ECG changes:

Start with loop diuretics if adequate renal function 1
Initiate potassium binder to allow eventual resumption of ACE inhibitor 1
Reserve dialysis for severe cases unresponsive to medical management 1

Patients with Cardiovascular Disease

Never permanently discontinue RAAS inhibitors—use potassium binders to maintain these life-saving medications. 1 Temporary dose reduction at K+ 6.2 mEq/L, then restart at lower dose with concurrent binder therapy. 1

Critical Pitfalls to Avoid

Never delay treatment while waiting for repeat lab confirmation if ECG changes present 1
Never use sodium bicarbonate without metabolic acidosis—it is ineffective without acidosis 1
Never give insulin without glucose—hypoglycemia is life-threatening 1, 2
Remember calcium, insulin, and beta-agonists are temporizing only—they do NOT remove potassium from the body 1, 2
Do not rely solely on ECG findings—they are variable and less sensitive than labs 1, 2
Do not permanently discontinue RAAS inhibitors—leads to worse cardiovascular and renal outcomes 1

Mild Hyperkalemia (5.0-5.5 mEq/L) Without ECG Changes

Do NOT initiate acute interventions (calcium, insulin, albuterol) for mild hyperkalemia without symptoms or ECG changes. 1

Management approach:

Review and eliminate contributing medications 1
Consider loop diuretics if adequate renal function 1
Avoid potassium supplements and salt substitutes 1
Dietary restriction has limited evidence and should be approached cautiously—potassium-rich diet provides cardiovascular benefits including blood pressure reduction 1

Team Approach

Optimal chronic hyperkalemia management involves a multidisciplinary team: cardiologists, nephrologists, primary care physicians, nurses, pharmacists, social workers, and dietitians. 3, 1 Educational initiatives on newer potassium binders are needed, especially in regions where specialist services may not be readily available. 3

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