What is the management of hyperkalemia?

Management of Hyperkalemia

For acute hyperkalemia with ECG changes or potassium ≥6.5 mEq/L, immediately administer IV calcium for cardiac membrane stabilization, followed by insulin with glucose and nebulized albuterol to shift potassium intracellularly, then initiate definitive potassium removal with loop diuretics or hemodialysis. 1

Classification and Initial Assessment

Hyperkalemia severity determines treatment urgency:

• Mild: 5.0-5.9 mEq/L 2, 1
• Moderate: 6.0-6.4 mEq/L 2, 1
• Severe: ≥6.5 mEq/L (life-threatening) 2, 1

Critical pitfall: ECG changes (peaked T waves, flattened P waves, prolonged PR interval, widened QRS) mandate urgent treatment regardless of potassium level. 1 However, ECG findings are highly variable and less sensitive than laboratory values—do not rely solely on ECG. 2, 3

Before initiating aggressive treatment, exclude pseudo-hyperkalemia from hemolysis, repeated fist clenching, or improper phlebotomy technique by repeating measurement with appropriate arterial sampling if suspected. 2, 1

Acute Management Algorithm

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

Administer IV calcium immediately if ECG changes present or K+ ≥6.5 mEq/L:

• Calcium chloride 10%: 5-10 mL (500-1000 mg) IV over 2-5 minutes (preferred for central access) 1
• Calcium gluconate 10%: 15-30 mL IV over 2-5 minutes (use for peripheral access due to lower tissue injury risk) 1

Effects begin within 1-3 minutes but last only 30-60 minutes. 1, 3 Calcium does NOT lower potassium—it only stabilizes cardiac membranes temporarily. 1 Repeat dosing may be necessary if no ECG improvement within 5-10 minutes. 3 Monitor heart rate continuously and stop if symptomatic bradycardia occurs. 1

Step 2: Shift Potassium Intracellularly (Onset: 15-30 minutes, Duration: 4-6 hours)

Administer all three agents together for maximum effect:

• Insulin with glucose: 10 units regular insulin IV with 25g dextrose (50 mL D50W) over 15-30 minutes 1, 3

  • Critical: Always give glucose with insulin to prevent life-threatening hypoglycemia 3
  • Monitor glucose and potassium every 2-4 hours 3
  • Can repeat every 4-6 hours if hyperkalemia persists 3

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

  • Reduces potassium by 0.5-1.0 mEq/L 1
  • Effects last 2-4 hours 3

• Sodium bicarbonate: 50 mEq IV over 5 minutes ONLY if concurrent metabolic acidosis present (pH <7.35, bicarbonate <22 mEq/L) 1, 3

  • Critical pitfall: Do NOT use without metabolic acidosis—it is ineffective and wastes time 3
  • Effects take 30-60 minutes to manifest 3

Warning: These are temporizing measures only—they do NOT remove potassium from the body. Rebound hyperkalemia can occur after 2 hours. 2, 1

Step 3: Eliminate Potassium from Body

Choose based on renal function and clinical urgency:

• Loop diuretics: Furosemide 40-80 mg IV to increase renal potassium excretion 1, 3

  • Effective only in patients with adequate kidney function (eGFR >30 mL/min) 2, 3

• Hemodialysis: Most reliable and effective method for severe hyperkalemia, especially with renal failure, oliguria, or cases refractory to medical management 1, 3, 4

• Potassium binders (for subacute/chronic management):

  • Sodium zirconium cyclosilicate (SZC/Lokelma): 10g three times daily for 48 hours, then 5-15g once daily for maintenance (onset: 1 hour) 2, 3
  • Patiromer (Veltassa): 8.4g once daily, titrated up to 25.2g daily (onset: ~7 hours) 2, 3
  • Sodium polystyrene sulfonate (Kayexalate): 15-50g orally or rectally—NOT recommended for acute management due to delayed onset and risk of bowel necrosis 1, 3, 5

Chronic Hyperkalemia Management

Medication Review and Optimization

Identify and eliminate contributing medications:

• NSAIDs, trimethoprim, heparin, beta-blockers, potassium-sparing diuretics, potassium supplements, salt substitutes 2, 3

Critical principle: Do NOT permanently discontinue RAAS inhibitors (ACE inhibitors, ARBs, mineralocorticoid antagonists) in patients with cardiovascular disease, heart failure, or proteinuric CKD—these provide mortality benefit and slow disease progression. 2, 3

RAAS Inhibitor Management Algorithm

For patients on RAAS inhibitors:

• K+ 4.5-5.0 mEq/L: Initiate/uptitrate RAAS inhibitor therapy with close monitoring 2, 3

• K+ 5.0-6.5 mEq/L: Initiate newer potassium binder (patiromer or SZC) while maintaining RAAS inhibitor therapy 2, 3

• K+ >6.5 mEq/L: Temporarily discontinue or reduce RAAS inhibitor, initiate potassium binder, then restart RAAS inhibitor at lower dose once K+ <5.5 mEq/L 2, 3

Long-Term Potassium Binder Therapy

Newer agents are preferred over sodium polystyrene sulfonate:

• Patiromer: Start 8.4g once daily, titrate to 25.2g based on potassium levels 2, 3
• Sodium zirconium cyclosilicate: 10g three times daily for 48 hours, then 5-15g once daily 2, 3

These agents enable optimization of RAAS inhibitor therapy and reduce cardiovascular and renal mortality. 2, 3

Monitoring Protocol

Frequency based on risk factors:

• Check potassium within 1 week of starting or escalating RAAS inhibitors 2, 3
• Reassess 7-10 days after initiating potassium binder therapy 2, 3
• High-risk patients (CKD, heart failure, diabetes, history of hyperkalemia): More frequent monitoring required 2
• After acute resolution: Monitor every 2-4 hours initially, then individualize based on stability 3

Monitor closely for hypokalemia in patients on potassium binders—overcorrection may be more dangerous than hyperkalemia. 3

Special Population Considerations

Chronic Kidney Disease

• 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 2, 3
• Patients with CKD tolerate higher potassium levels due to compensatory mechanisms 2
• Maintain RAAS inhibitors aggressively in proteinuric CKD using potassium binders—these drugs slow CKD progression 3

Cardiovascular Disease

• U-shaped curve exists between serum potassium and mortality—both hyperkalemia and hypokalemia increase risk 2
• Patients with atrioventricular heart block may experience worsening cardiac symptoms at lower potassium concentrations 2
• Rate of potassium increase matters—rapid rise more likely to cause cardiac abnormalities than slow steady rise 2

Dietary Considerations

Evidence linking dietary potassium intake to serum levels is limited. 2, 3 A potassium-rich diet provides cardiovascular benefits including blood pressure reduction. 2, 3 Stringent dietary restrictions may not be necessary in patients receiving newer potassium binders, though this requires further study. 2

Key Clinical Pitfalls to Avoid

• Never delay treatment while waiting for repeat lab confirmation if ECG changes present 3
• Never give insulin without glucose—hypoglycemia can be life-threatening 3
• Never use sodium bicarbonate without metabolic acidosis 3
• Remember calcium, insulin, and beta-agonists are temporizing only—they do NOT remove potassium 3
• Do not permanently discontinue RAAS inhibitors—use potassium binders to maintain these life-saving medications 2, 3
• Avoid sodium polystyrene sulfonate for acute management due to delayed onset and bowel necrosis risk 1, 3