What is the treatment for a patient with hyperkalemia?

Treatment of Hyperkalemia

Immediate Assessment and Severity Classification

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

• Obtain an ECG immediately to identify peaked T waves, flattened P waves, prolonged PR interval, or widened QRS complexes—these findings indicate urgent cardiac membrane stabilization is required 1, 2
• Exclude pseudohyperkalemia from hemolysis, repeated fist clenching, or poor phlebotomy technique by repeating the measurement with proper technique or arterial sampling before initiating aggressive treatment 1, 2

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

For severe hyperkalemia (K+ ≥6.5 mEq/L) or ANY ECG changes, administer intravenous calcium immediately to prevent fatal arrhythmias. 1, 2, 3

• Calcium chloride (10%): 5-10 mL (500-1000 mg) IV over 2-5 minutes is preferred for rapid cardiac protection, providing higher ionized calcium concentrations than calcium gluconate 1, 3
• Calcium gluconate (10%): 15-30 mL IV over 2-5 minutes is an acceptable alternative, particularly when only peripheral IV access is available 1, 2
• Administer through a central venous catheter when possible, as calcium chloride extravasation through peripheral IV can cause severe tissue injury 1
• Monitor heart rate continuously during administration and stop if symptomatic bradycardia occurs 1
• Critical caveat: 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 calcium dose immediately 2

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

Administer all three agents simultaneously for maximum potassium-lowering effect: 1, 2

• Insulin with glucose: 10 units regular insulin IV with 25g glucose (50 mL of D50W) over 15-30 minutes is the most effective intracellular shift agent 1, 2, 3

  • Verify baseline glucose is not below 3.3 mEq/L before administering insulin 2
  • Monitor glucose every 2-4 hours after administration to prevent hypoglycemia 2
  • Patients with low baseline glucose, no diabetes history, female sex, and altered renal function are at highest risk for hypoglycemia 2
  • Insulin can be repeated every 4-6 hours if hyperkalemia persists, with careful glucose and potassium monitoring 2

• Nebulized albuterol: 10-20 mg over 15 minutes as adjunctive therapy to augment insulin's effect 1, 2, 3

  • Reduces serum potassium by approximately 0.5-1.0 mEq/L 1
  • Effects last 2-4 hours with potential for rebound hyperkalemia 1, 2

• Sodium bicarbonate: 50 mEq IV over 5 minutes ONLY if metabolic acidosis is present (pH <7.35, bicarbonate <22 mEq/L) 1, 2

  • Do not use in patients without metabolic acidosis—it is ineffective and wastes time 2
  • Effects take 30-60 minutes to manifest 2

Critical warning: These are temporizing measures only—rebound hyperkalemia can occur within 2-4 hours, requiring definitive potassium removal strategies. 1, 2

Step 3: Eliminate Potassium from Body (Definitive Treatment)

For Acute Management:

• Loop diuretics (furosemide 40-80 mg IV) to increase renal potassium excretion in patients with adequate kidney function (eGFR >30 mL/min) 1, 2, 3

  • Titrate to maintain euvolemia, not primarily for potassium management 2

• Hemodialysis is the most effective and reliable method for severe hyperkalemia, especially in patients with renal failure, oliguria, or cases refractory to medical management 1, 2, 3

  • Monitor for rebound hyperkalemia within 4-6 hours post-dialysis as intracellular potassium redistributes 2

For Subacute to Chronic Management:

Newer potassium binders are strongly preferred over sodium polystyrene sulfonate (Kayexalate) due to superior safety profiles. 1, 2

• Sodium zirconium cyclosilicate (SZC/Lokelma): 10g three times daily for 48 hours, then 5-15g once daily for maintenance 1, 2

  • Onset of action: ~1 hour, making it suitable for urgent outpatient scenarios 2
  • Monitor for edema due to sodium content 2

• Patiromer (Veltassa): 8.4g once daily with food, titrated up to 25.2g daily based on potassium response 1, 2

  • Onset of action: ~7 hours 2
  • Separate from other oral medications by at least 3 hours (6 hours in gastroparesis) 4
  • Monitor magnesium levels as patiromer causes hypomagnesemia 2

• Sodium polystyrene sulfonate (Kayexalate): 15-50g orally or rectally should be avoided due to delayed onset, risk of intestinal necrosis, colonic necrosis, and doubling of serious gastrointestinal adverse events 1, 2, 4

  • FDA limitation: Should NOT be used as emergency treatment for life-threatening hyperkalemia due to delayed onset of action 4
  • Concomitant sorbitol administration is contraindicated due to increased necrosis risk 4

Treatment Algorithm by Severity

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

1. Calcium chloride 10%: 5-10 mL IV over 2-5 minutes immediately 1, 3
2. Within 15 minutes, give all three simultaneously:
   • Insulin 10 units + glucose 25g IV 1, 3
   • Albuterol 10-20 mg nebulized 1, 3
   • Sodium bicarbonate 50 mEq IV (only if acidotic) 1
3. Initiate definitive removal: Loop diuretics or hemodialysis 1, 3
4. For patients on RAAS inhibitors: Temporarily discontinue or reduce until K+ <5.5 mEq/L, then restart at lower dose with concurrent potassium binder 2, 3

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

1. Insulin/glucose and albuterol for intracellular shift 1, 3
2. Loop diuretics if adequate renal function 1, 3
3. Initiate potassium binder (SZC or patiromer) 1, 3
4. Review and adjust contributing medications 1, 3

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

1. Review and discontinue offending medications: NSAIDs, trimethoprim, heparin, beta-blockers, potassium supplements, salt substitutes 1, 2, 3
2. Initiate potassium binder for chronic management 1, 3
3. Maintain RAAS inhibitor therapy—do NOT discontinue 1, 3
4. Loop or thiazide diuretics to promote urinary excretion 2

Management of Chronic/Recurrent Hyperkalemia in Patients on RAAS Inhibitors

For patients with cardiovascular disease, heart failure, or proteinuric CKD requiring RAAS inhibitors, maintaining these life-saving medications using potassium binders is preferable to discontinuation. 1, 2, 3

• For K+ 5.0-6.5 mEq/L: Initiate approved potassium-lowering agent (patiromer or SZC) and maintain RAAS inhibitor therapy unless alternative treatable cause identified 1, 2, 3
• For K+ >6.5 mEq/L: Temporarily discontinue or reduce RAAS inhibitor, initiate potassium-lowering agent when levels >5.0 mEq/L, monitor closely, then restart RAAS inhibitor at lower dose once K+ <5.5 mEq/L 1, 2, 3
• Check potassium within 7-10 days after starting or increasing RAAS inhibitor doses 2
• The triple combination of ACE inhibitor + ARB + MRA is NOT recommended due to excessive hyperkalemia risk 2

Monitoring Protocol

• High-risk patients (CKD, diabetes, heart failure, history of hyperkalemia) require checking potassium within 1 week of starting or escalating RAAS inhibitors 2
• After initiating potassium binder therapy, reassess at 7-10 days 2
• For patients on insulin therapy for hyperkalemia, monitor potassium every 2-4 hours initially 2
• Monitor magnesium levels in patients on patiromer to detect hypomagnesemia 2

Critical Pitfalls to Avoid

• Never delay calcium administration while waiting for repeat potassium levels if ECG changes are present—ECG changes indicate urgent need regardless of exact potassium value 2
• Never rely solely on ECG findings—they are highly variable and less sensitive than laboratory tests 2
• Never give insulin without glucose—hypoglycemia can be life-threatening 2
• Never use sodium bicarbonate without metabolic acidosis—it is ineffective in non-acidotic patients 1, 2
• Never administer calcium through the same IV line as sodium bicarbonate—precipitation will occur 2
• Remember that calcium, insulin, and beta-agonists do NOT remove potassium from the body—they only temporize, requiring concurrent definitive removal strategies 1, 2
• Never permanently discontinue RAAS inhibitors in patients with cardiovascular disease or proteinuric CKD—use potassium binders instead to maintain these mortality-reducing medications 1, 2, 3