Hyperkalemia Management

Severity Classification and Initial Assessment

Hyperkalemia severity determines your treatment approach: mild (5.0-5.9 mEq/L), moderate (6.0-6.4 mEq/L), or severe (≥6.5 mEq/L), with ECG changes mandating urgent treatment regardless of the potassium level. 1, 2, 3

Before initiating aggressive treatment, exclude pseudo-hyperkalemia from hemolysis, repeated fist clenching, or improper blood sampling by repeating the measurement with appropriate technique or arterial sampling 3
ECG changes indicating urgent treatment include peaked T waves, flattened P waves, prolonged PR interval, and widened QRS complexes 1, 2, 3
Critical pitfall: ECG findings can be highly variable and less sensitive than laboratory tests, but absent or atypical ECG changes do not exclude the necessity for immediate intervention 3, 4

Acute Management Algorithm

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

For severe hyperkalemia (≥6.5 mEq/L) OR any ECG changes, administer IV calcium immediately to protect against arrhythmias. 1, 2, 3

Preferred agent: Calcium chloride (10%): 5-10 mL (500-1000 mg) IV over 2-5 minutes provides more rapid increase in ionized calcium than calcium gluconate 1, 3
Alternative: Calcium gluconate (10%): 15-30 mL IV over 2-5 minutes if peripheral IV access only 1, 2
Administer calcium chloride through a central venous catheter when possible, as extravasation through peripheral IV may cause severe skin and soft tissue injury 1
Monitor heart rate continuously during administration and stop if symptomatic bradycardia occurs 1
Critical understanding: Calcium does NOT lower serum potassium—it only stabilizes cardiac membranes temporarily for 30-60 minutes 1, 2, 3
If no ECG improvement within 5-10 minutes, repeat the dose: 15-30 mL of calcium gluconate IV over 2-5 minutes 3
Never administer calcium through the same IV line as sodium bicarbonate, as precipitation will occur 3

Step 2: Shift Potassium into Cells (Onset 15-30 Minutes, Duration 4-6 Hours)

Administer all three agents together for maximum effect in severe hyperkalemia: 3

Insulin with glucose: 10 units regular insulin IV with 25g glucose (50 mL of D50W) over 15-30 minutes 1, 2, 3
- Verify potassium is not below 3.3 mEq/L before administering insulin 3
- Monitor glucose closely to prevent hypoglycemia, particularly in patients with low baseline glucose, no diabetes history, female sex, and altered renal function 3
- Can be repeated every 4-6 hours as needed, carefully monitoring serum potassium and glucose levels 3
Nebulized beta-2 agonist: Albuterol 10-20 mg in 4 mL nebulized over 15 minutes 1, 2, 3
- Reduces serum potassium by approximately 0.5-1.0 mEq/L 1, 2
- Effects are temporary (2-4 hours) and rebound hyperkalemia can occur 1, 3
Sodium bicarbonate: 50 mEq IV over 5 minutes ONLY if metabolic acidosis is present (pH <7.35, bicarbonate <22 mEq/L) 1, 2, 3
- Critical pitfall: Do not use sodium bicarbonate in patients without metabolic acidosis—it is ineffective and wastes time 3
- Effects take 30-60 minutes to manifest 3

Step 3: Eliminate Potassium from Body (Definitive Treatment)

Choose based on renal function and clinical urgency: 1, 2, 3

Loop diuretics: Furosemide 40-80 mg IV to increase urinary potassium excretion, effective only in patients with adequate renal function 1, 2, 3
- Titrate to maintain euvolemia, not primarily for potassium management 3
Hemodialysis: Most effective and reliable method for severe hyperkalemia, especially in renal failure, oliguria, or cases unresponsive to medical management 1, 2, 3
- Monitor for rebound hyperkalemia within 4-6 hours post-dialysis as intracellular potassium redistributes 3
Newer potassium binders (preferred for subacute/chronic management):
- Sodium zirconium cyclosilicate (SZC/Lokelma): 10 g three times daily for 48 hours, then 5-15 g once daily for maintenance 1, 2, 3
  - Onset of action: ~1 hour, making it suitable for more urgent scenarios 3, 5
  - Each 5 g dose contains approximately 400 mg sodium; monitor for edema, particularly in heart failure or renal disease 5
  - Separate from other oral medications by at least 2 hours before or after due to transient increase in gastric pH 5
- Patiromer (Veltassa): 8.4 g once daily with food, titrated up to 25.2 g daily based on potassium levels 1, 2, 3
  - Onset of action: ~7 hours 3
  - Separate from other oral medications by at least 3 hours 3
  - Monitor magnesium levels as patiromer causes hypomagnesemia 3
Avoid sodium polystyrene sulfonate (Kayexalate): Associated with delayed onset of action, risk of bowel necrosis, intestinal ischemia, colonic necrosis, and doubling of risk for serious gastrointestinal adverse events 2, 3

Medication Management During Acute Episode

Temporarily discontinue or reduce contributing medications when potassium >6.5 mEq/L: 3

RAAS inhibitors (ACE inhibitors, ARBs, mineralocorticoid receptor antagonists) 3
NSAIDs 3
Potassium-sparing diuretics (spironolactone, amiloride, triamterene) 3
Trimethoprim 3
Heparin 3
Beta-blockers 3
Potassium supplements and salt substitutes 3

Critical principle: For patients with cardiovascular disease or proteinuric CKD, do NOT permanently discontinue RAAS inhibitors—temporarily hold or reduce, then restart at lower dose once potassium <5.0 mEq/L with concurrent potassium binder therapy 3

Chronic/Recurrent Hyperkalemia Management

For Patients on RAAS Inhibitors with Potassium 5.0-6.5 mEq/L:

Initiate a potassium binder while maintaining RAAS inhibitor therapy—do not discontinue these life-saving medications. 1, 2, 3

Start sodium zirconium cyclosilicate 10 g three times daily for 48 hours, then 5-15 g once daily 3
OR start patiromer 8.4 g once daily, titrated based on response 3
RAAS inhibitors provide mortality benefit in cardiovascular and renal disease and slow CKD progression 1, 3
Check potassium within 1 week of starting or escalating RAAS inhibitors 3
Reassess potassium 7-10 days after initiating potassium binder therapy 3

For Patients with Potassium >6.5 mEq/L:

Temporarily discontinue or reduce RAAS inhibitor 1, 2, 3
Initiate potassium-lowering agent when levels >5.0 mEq/L 1, 3
Monitor potassium levels closely 1, 3
Restart RAAS inhibitor at lower dose once potassium <5.0 mEq/L with concurrent potassium binder 3

Optimize Diuretic Therapy:

Add loop diuretic (furosemide 40-80 mg daily) to increase urinary potassium excretion if adequate renal function present 3

Monitoring Protocol

Check potassium within 1 week of starting or escalating RAAS inhibitors 3
Reassess 7-10 days after dose changes, especially in high-risk patients with CKD, heart failure, or diabetes 3
For severe initial hyperkalemia (>6.5 mEq/L), monitor every 2-4 hours initially due to risk of rebound 3
Individualize monitoring frequency based on eGFR, heart failure, diabetes, or history of hyperkalemia 3
Monitor magnesium levels in patients on patiromer 3
Monitor for edema in patients on sodium zirconium cyclosilicate 5

Special Population Considerations

CKD Patients:

Optimal potassium range is broader in advanced CKD: 3.3-5.5 mEq/L for stage 4-5 CKD versus 3.5-5.0 mEq/L for stage 1-2 CKD 3
Maintain RAAS inhibitors aggressively in proteinuric CKD using potassium binders, as these drugs slow CKD progression 3
Target predialysis potassium of 4.0-5.5 mEq/L to minimize mortality risk 3

Hemodialysis Patients:

Start sodium zirconium cyclosilicate 5 g once daily on non-dialysis days, adjust weekly in 5 g increments based on predialysis potassium 3
OR start patiromer 8.4 g once daily with food, separated from other medications by at least 3 hours 3
Patients on hemodialysis may be prone to acute illness that can increase risk of hypokalemia on potassium binders 5
Consider adjusting dialysate potassium concentration (typically 2.0-3.0 mEq/L) based on predialysis levels 3

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 3
Never rely solely on ECG findings—they are highly variable and less sensitive than laboratory tests 3
Never use sodium bicarbonate without metabolic acidosis—it is ineffective and wastes time 3
Never give insulin without glucose—hypoglycemia can be life-threatening 3
Remember that calcium, insulin, and beta-agonists are temporizing measures only—they do NOT remove potassium from the body 3
Failure to initiate concurrent potassium-lowering therapies will result in recurrent life-threatening arrhythmias within 30-60 minutes 3
Do not permanently discontinue RAAS inhibitors in patients with cardiovascular disease or proteinuric CKD—use potassium binders instead 3

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