Treatment of Hyperkalemia
Immediate Assessment and Severity Classification
For hyperkalemia, immediately assess severity and ECG changes to determine urgency of treatment, as ECG changes mandate urgent intervention regardless of potassium level.
- Classify hyperkalemia as mild (5.0-5.9 mEq/L), moderate (6.0-6.4 mEq/L), or severe (≥6.5 mEq/L) 1, 2
- Any ECG changes (peaked T waves, flattened P waves, prolonged PR interval, widened QRS) indicate a medical emergency requiring immediate treatment regardless of potassium level 1, 2
- Verify the result is not pseudohyperkalemia from hemolysis, repeated fist clenching, or poor phlebotomy technique before initiating aggressive treatment 1, 2
Acute Treatment Algorithm
Step 1: Cardiac Membrane Stabilization (Immediate - Within 1-3 Minutes)
Administer intravenous calcium immediately for any patient with ECG changes or severe hyperkalemia (K+ ≥6.5 mEq/L).
- Calcium chloride (10%): 5-10 mL (500-1000 mg) IV over 2-5 minutes is preferred as it provides more rapid increase in ionized calcium than calcium gluconate 1, 3
- Calcium gluconate (10%): 15-30 mL IV over 2-5 minutes is an alternative, particularly for peripheral IV access 1, 2
- Effects begin within 1-3 minutes but last only 30-60 minutes 1, 2
- Critical caveat: Calcium does not lower serum potassium—it only protects against arrhythmias 1, 3
- Repeat dosing may be necessary if no ECG improvement within 5-10 minutes 2
- Monitor heart rate during administration and stop if symptomatic bradycardia occurs 1
Step 2: Shift Potassium into Cells (Onset 15-30 Minutes, Duration 4-6 Hours)
Administer insulin with glucose AND nebulized albuterol simultaneously for maximum potassium-lowering effect.
- Insulin 10 units regular insulin IV with 25g glucose (50 mL of D50W) over 15-30 minutes 1, 2, 3
- Verify glucose is not below 3.3 mEq/L before administering insulin 2
- Monitor glucose every 2-4 hours after administration to prevent hypoglycemia 2
- Nebulized albuterol 10-20 mg over 15 minutes as adjunctive therapy 1, 2, 3
- Effects begin within 15-30 minutes and last 4-6 hours 1, 2
- Sodium bicarbonate 50 mEq IV over 5 minutes ONLY if concurrent metabolic acidosis is present (pH <7.35, bicarbonate <22 mEq/L) 1, 2, 3
- Do not use sodium bicarbonate in patients without metabolic acidosis—it is ineffective and potentially harmful 2, 3
Important: These measures are temporary and rebound hyperkalemia can occur after 2 hours 1, 2
Step 3: Eliminate Potassium from Body (Definitive Treatment)
Initiate potassium elimination measures immediately after temporizing treatments.
- Loop diuretics (furosemide 40-80 mg IV) if adequate renal function exists (eGFR >30 mL/min) 1, 2, 3
- Hemodialysis is the most effective method for severe hyperkalemia, especially in renal failure, oliguria, or cases unresponsive to medical management 1, 2, 3
- Newer potassium binders (patiromer or sodium zirconium cyclosilicate) are preferred over sodium polystyrene sulfonate for subacute to chronic management 1, 2, 3
Chronic and Recurrent Hyperkalemia Management
For Patients on RAAS Inhibitors (ACE Inhibitors, ARBs, Mineralocorticoid Antagonists)
Do not discontinue RAAS inhibitors in patients with cardiovascular disease or CKD—instead, initiate potassium binders to maintain these life-saving medications.
Potassium 5.0-6.4 mEq/L:
- Initiate approved potassium-lowering agent (patiromer or sodium zirconium cyclosilicate) while maintaining RAAS inhibitor therapy 1, 2, 3
- Eliminate contributing medications: NSAIDs, trimethoprim, heparin, potassium supplements, salt substitutes 2
- Optimize diuretic therapy with loop or thiazide diuretics 2, 3
Potassium >6.5 mEq/L:
- Temporarily discontinue or reduce RAAS inhibitor dose 1, 2
- Initiate potassium-lowering agent when levels >5.0 mEq/L 1, 2
- Restart RAAS inhibitor at lower dose once potassium controlled with concurrent potassium binder therapy 2
Potassium Binder Options
Sodium zirconium cyclosilicate (SZC/Lokelma) is preferred for faster onset; patiromer for once-daily dosing.
- Sodium zirconium cyclosilicate (SZC): 10g three times daily for 48 hours, then 5-15g once daily for maintenance 2, 3
- Patiromer (Veltassa): 8.4g once daily, titrated up to 25.2g daily based on potassium levels 2, 3
- Onset of action: ~7 hours 2
- Administer at least 3 hours before or after other oral medications (6 hours for patients with gastroparesis) 4
- Sodium polystyrene sulfonate (Kayexalate) should be avoided due to delayed onset, risk of bowel necrosis, and poor efficacy 2, 4, 5
Monitoring Protocol
Check potassium within 1 week of starting or escalating RAAS inhibitors, then reassess 7-10 days after any dose changes.
- Monitor potassium and renal function at 1-2 weeks, 3 months, then every 6 months for patients on RAAS inhibitors 2
- More frequent monitoring required in high-risk patients: CKD, heart failure, diabetes, history of hyperkalemia 2, 3
- For patients on potassium binders, monitor closely for both efficacy and hypokalemia 2
- Optimal potassium range varies by CKD stage: 3.5-5.0 mEq/L for stage 1-2 CKD; 3.3-5.5 mEq/L for stage 4-5 CKD 2
Critical Pitfalls to Avoid
- Do not rely solely on ECG findings—they are highly variable and less sensitive than laboratory tests 2
- Do not use sodium bicarbonate without concurrent metabolic acidosis 2, 3
- Always administer glucose with insulin to prevent hypoglycemia 2, 3
- Remember that calcium, insulin, and beta-agonists do not remove potassium—they only temporize 2, 3
- Do not discontinue RAAS inhibitors permanently in patients with cardiovascular disease or proteinuric CKD—this leads to worse outcomes 1, 2
- Avoid sodium polystyrene sulfonate with sorbitol due to risk of intestinal necrosis 4
- Do not use sodium polystyrene sulfonate as emergency treatment due to delayed onset of action 4
Special Populations
Patients with CKD:
- Maintain RAAS inhibitors aggressively using potassium binders, as these drugs slow CKD progression 2
- Dialysis is reserved for severe cases unresponsive to medical management 2, 3