What is the treatment for hyperkalemia?

Treatment of Hyperkalemia

For severe hyperkalemia (≥6.5 mEq/L) or any ECG changes, immediately administer IV calcium chloride 10% (5-10 mL over 2-5 minutes) to stabilize the cardiac membrane, followed simultaneously by insulin 10 units with 25g glucose and nebulized albuterol 10-20 mg to shift potassium intracellularly, then initiate definitive potassium removal with loop diuretics or hemodialysis. 1, 2, 3

Severity Classification and Initial Assessment

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

Critical caveat: ECG changes (peaked T waves, flattened P waves, prolonged PR interval, widened QRS) mandate urgent treatment regardless of the potassium level—absent ECG changes do NOT exclude the need for immediate intervention. 1, 2, 4

Before initiating aggressive treatment, exclude pseudo-hyperkalemia from hemolysis or improper sampling by repeating the measurement with appropriate technique or arterial sampling. 1, 2

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

Calcium chloride is superior to calcium gluconate because it provides more rapid increase in ionized calcium concentration, making it more effective in critically ill patients. 1

• Preferred: Calcium chloride 10%: 5-10 mL (500-1000 mg) IV over 2-5 minutes 1, 2, 3
• Alternative: Calcium gluconate 10%: 15-30 mL IV over 2-5 minutes 1, 2
• Pediatric dose: Calcium chloride 20 mg/kg (0.2 mL/kg of 10% solution) over 5-10 minutes 1

Onset: 1-3 minutes; Duration: 30-60 minutes (temporary only) 1, 2

Critical monitoring: Continuous ECG monitoring is mandatory during and for 5-10 minutes after administration; stop if symptomatic bradycardia occurs. 1, 2 If no ECG improvement within 5-10 minutes, repeat the dose. 1, 2

Important limitations: Calcium does NOT lower serum potassium—it only stabilizes cardiac membranes temporarily. 1, 2, 3 Administer through central line when possible due to tissue injury risk with peripheral extravasation. 1 Never give calcium through the same IV line as sodium bicarbonate (causes precipitation). 2

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

Give all three agents together for maximum effect in severe hyperkalemia: 2

Insulin with Glucose (First-line)

• Standard dose: 10 units regular insulin IV with 25g glucose (50 mL of D50W) over 15-30 minutes 1, 2, 3
• Alternative glucose formulations: 100 mL of D25W or 500 mL of D5W (though D50W is preferred for concentrated delivery) 1
• Pediatric dose: 200 mg/kg as D10W 1
• Onset: 15-30 minutes; Duration: 4-6 hours 1, 2

Critical safety: Always verify potassium is not below 3.3 mEq/L before giving insulin. 2 Monitor glucose closely—patients with low baseline glucose, no diabetes, female sex, and renal dysfunction are at highest risk for hypoglycemia. 2 Can repeat every 4-6 hours if hyperkalemia persists, with careful glucose and potassium monitoring every 2-4 hours. 2

Nebulized Beta-2 Agonist (Adjunctive)

• Dose: Albuterol 10-20 mg nebulized over 15 minutes 1, 2, 3
• Mechanism: Stimulates Na+/K+-ATPase pump, promoting potassium shift into cells 1
• Onset: 15-30 minutes; Duration: 2-4 hours 1, 2
• Expected effect: Reduces serum potassium by approximately 0.5-1.0 mEq/L 1

Sodium Bicarbonate (ONLY if Metabolic Acidosis Present)

• Dose: 50 mEq IV over 5 minutes 1, 2
• Indication: Use ONLY in patients with concurrent metabolic acidosis (pH <7.35, bicarbonate <22 mEq/L) 1, 2
• Onset: 30-60 minutes (slower than insulin/albuterol) 2
• Mechanism: Increases distal sodium delivery and counters acidosis-induced potassium release 2

Critical pitfall: Sodium bicarbonate is ineffective and wastes time in patients without metabolic acidosis—do not use routinely. 2

Step 3: Eliminate Potassium from Body (Definitive Treatment)

Loop Diuretics (If Adequate Renal Function)

• Dose: Furosemide 40-80 mg IV 1, 2, 3
• Mechanism: Increases renal potassium excretion by stimulating flow to collecting ducts 2
• Limitation: Effective only in patients with preserved kidney function 1, 2, 3
• Important: Titrate to maintain euvolemia, not primarily for potassium management 2

Potassium Binders (Subacute to Chronic Management)

Newer agents are strongly preferred over sodium polystyrene sulfonate (Kayexalate) due to safety concerns including intestinal ischemia, colonic necrosis, and doubling of serious GI adverse events. 2, 5

Sodium Zirconium Cyclosilicate (SZC/Lokelma) - Preferred for Urgent Scenarios

• Acute dosing: 10g three times daily for 48 hours 1, 2
• Maintenance: 5-15g once daily 1, 2
• Onset: ~1 hour (fastest-acting binder) 1, 2
• Mechanism: Exchanges hydrogen and sodium for potassium 2
• Monitoring: Watch for edema due to sodium content 2

Patiromer (Veltassa) - Preferred for Chronic Management

• Starting dose: 8.4g once daily with food 1, 2
• Titration: Up to 25.2g daily based on potassium response 1, 2
• Onset: ~7 hours 1, 2
• Mechanism: Exchanges calcium for potassium in colon 2
• Critical administration: Separate from other oral medications by at least 3 hours 2
• Monitoring: Check magnesium levels (causes hypomagnesemia); for each 1 mEq/L increase in magnesium, potassium increases by 1.07 mEq/L 2

Sodium Polystyrene Sulfonate (Kayexalate) - Avoid

• FDA indication: Treatment of hyperkalemia, but NOT for emergency use due to delayed onset 5
• Major safety concerns: Associated with intestinal ischemia, colonic necrosis, and serious GI adverse events 2
• Recommendation: Avoid in favor of newer potassium binders 1, 2

Hemodialysis (Most Effective for Severe Cases)

• Indications: Severe hyperkalemia unresponsive to medical management, oliguria, end-stage renal disease 1, 2, 3
• Efficacy: Most effective and reliable method for potassium removal 1, 2, 6
• Post-dialysis monitoring: Potassium can rebound within 4-6 hours as intracellular potassium redistributes; monitor every 2-4 hours initially in severe cases 2

Treatment Algorithm by Severity

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

1. Immediate (0-5 minutes): Calcium chloride 10%: 5-10 mL IV over 2-5 minutes with continuous ECG monitoring 1, 2, 3
2. Within 15 minutes: Give all three simultaneously:
   • Insulin 10 units + glucose 25g IV 1, 2, 3
   • Albuterol 10-20 mg nebulized 1, 2, 3
   • Sodium bicarbonate 50 mEq IV ONLY if metabolic acidosis present 1, 2
3. Definitive removal: Loop diuretics (if renal function adequate) or hemodialysis 1, 2, 3
4. Medication review: Temporarily discontinue or reduce RAAS inhibitors, NSAIDs, potassium-sparing diuretics, trimethoprim, heparin, beta-blockers, potassium supplements, salt substitutes 2

Moderate Hyperkalemia (K+ 6.0-6.4 mEq/L Without ECG Changes)

1. Intracellular shift: Insulin/glucose + albuterol 1, 2, 3
2. Potassium removal: Loop diuretics or initiate potassium binder (SZC for faster effect, patiromer for chronic management) 1, 2
3. Medication review: Assess and adjust contributing medications 2

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

1. No acute interventions (calcium, insulin, albuterol) unless symptomatic 2
2. Medication review: Discontinue or reduce offending medications (NSAIDs, potassium supplements, salt substitutes) 1, 2, 3
3. Chronic management: Initiate potassium binder if recurrent or patient requires RAAS inhibitor therapy 1, 2, 3
4. Diuretics: Consider loop or thiazide diuretics if adequate renal function 2

Management of Chronic/Recurrent Hyperkalemia

Critical principle: Do NOT permanently discontinue RAAS inhibitors (ACE inhibitors, ARBs, mineralocorticoid antagonists) in patients with cardiovascular disease or proteinuric CKD—these provide mortality benefit and slow disease progression. 1, 2, 3

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

• Initiate approved potassium-lowering agent (patiromer or SZC) 1, 2, 3
• Maintain RAAS inhibitor therapy unless alternative treatable cause identified 1, 2
• Monitor potassium closely (within 7-10 days after starting or dose changes) 2

For Patients on RAAS Inhibitors with K+ >6.5 mEq/L:

• Temporarily discontinue or reduce RAAS inhibitor 1, 2
• Initiate potassium-lowering agent when levels >5.0 mEq/L 1, 2
• Restart RAAS inhibitor at lower dose once potassium <5.0-5.5 mEq/L with concurrent potassium binder 2

Medication Review (Priority Medications to Adjust):

• Discontinue: NSAIDs (impair renal potassium excretion), potassium supplements, salt substitutes (high potassium content) 2
• Avoid combinations: Triple therapy (ACE inhibitor + ARB + MRA) has excessive hyperkalemia risk 2
• Review: Potassium-sparing diuretics (amiloride, triamterene, spironolactone), trimethoprim, heparin, beta-blockers 2

Monitoring Protocol:

• Check potassium within 1 week of starting or escalating RAAS inhibitors 2
• Reassess 7-10 days after initiating potassium binder therapy 2
• More frequent monitoring (every 2-4 hours initially) for high-risk patients: CKD, heart failure, diabetes, history of severe hyperkalemia 2

Dietary Considerations:

• Evidence linking dietary potassium intake to serum levels is limited 2
• Potassium-rich diet provides cardiovascular benefits including blood pressure reduction 2
• Recommendation: Focus on reducing nonplant sources of potassium rather than stringent restriction; newer potassium binders may allow less restrictive diets 2, 7

Special Populations

Hemodialysis Patients:

• Target predialysis potassium: 4.0-5.5 mEq/L to minimize mortality risk 2
• First-line: SZC 5g once daily on non-dialysis days, adjust weekly in 5g increments 2
• Second-line: Patiromer 8.4g once daily, titrate to 16.8-25.2g based on response 2
• Dialysate adjustment: Consider lowering dialysate potassium to 2.0 mEq/L for recurrent severe hyperkalemia, but monitor for intradialytic arrhythmias 2

CKD Patients (Non-Dialysis):

• Patients with advanced CKD tolerate higher potassium levels (optimal range 3.3-5.5 mEq/L for stage 4-5 CKD) 2
• Maintain RAAS inhibitors aggressively using potassium binders—these drugs slow CKD progression 2
• Loop diuretics effective only if adequate kidney function present 2, 3

Critical Pitfalls to Avoid

• Never delay treatment while waiting for repeat labs if ECG changes are present—ECG changes indicate urgent need regardless of exact potassium value 2
• Never rely on calcium alone—it is temporizing only (30-60 minutes); failure to initiate concurrent potassium-lowering therapies results in recurrent life-threatening arrhythmias 2
• Never give insulin without glucose—hypoglycemia can be life-threatening 2
• Never use sodium bicarbonate without metabolic acidosis—it is ineffective and wastes time 2
• Remember: Calcium, insulin, and beta-agonists do NOT remove potassium from the body—they only temporize 2
• Do not rely solely on ECG findings—they are highly variable and less sensitive than laboratory tests 2
• Monitor for rebound hyperkalemia after temporary measures (insulin/glucose, albuterol)—effects last only 2-6 hours 1, 2