How to Lower Potassium Levels in the Blood
For acute severe hyperkalemia (≥6.5 mEq/L or ECG changes), immediately administer IV calcium gluconate 15-30 mL over 2-5 minutes to stabilize cardiac membranes, followed by insulin with glucose and nebulized albuterol to shift potassium intracellularly; for chronic management (5.0-6.5 mEq/L), initiate newer potassium binders (patiromer or sodium zirconium cyclosilicate) while maintaining RAAS inhibitor therapy. 1
Initial Assessment
Verify true hyperkalemia by excluding pseudohyperkalemia from hemolysis, repeated fist clenching, or poor phlebotomy technique before initiating treatment. 1, 2
Classify severity immediately:
Obtain ECG immediately to assess for peaked T waves, flattened P waves, prolonged PR interval, or widened QRS complexes—these findings mandate urgent treatment regardless of potassium level. 1, 2 ECG changes are highly variable and less sensitive than laboratory values, so do not rely solely on them. 1
Acute Management (K+ ≥6.5 mEq/L or ECG Changes)
Step 1: Cardiac Membrane Stabilization (Does NOT Lower Potassium)
Administer calcium gluconate 10% solution: 15-30 mL (1.5-3 grams) IV over 2-5 minutes to stabilize cardiac membranes. 3, 1, 2 Alternatively, use calcium chloride 10%: 5-10 mL IV over 2-5 minutes. 1
- Effects begin within 1-3 minutes but are temporary (30-60 minutes) 1, 2
- Does NOT reduce total body potassium 1
- Repeat dosing may be necessary if no ECG improvement within 5-10 minutes 1
- Continuous cardiac monitoring is mandatory during and after administration 1, 2
Critical caveat: In patients with malignant hyperthermia and hyperkalemia, calcium should only be used in extremis as it may contribute to calcium overload. 1
Step 2: Shift Potassium Intracellularly (Temporary, Does NOT Remove Potassium)
Administer insulin with glucose: 10 units regular insulin IV with 25-50 grams glucose (unless blood glucose >250 mg/dL). 3, 1 This is the most reliable agent for promoting transcellular shift. 4
- Effects begin within 15-30 minutes and last 4-6 hours 3, 1
- Monitor glucose closely to prevent hypoglycemia 1
- Can be repeated every 4-6 hours if hyperkalemia persists 1
- Verify potassium is not below 3.3 mEq/L before administering 1
Administer nebulized albuterol: 20 mg in 4 mL as adjunctive therapy. 1
Sodium bicarbonate: ONLY use in patients with concurrent metabolic acidosis (pH <7.35, bicarbonate <22 mEq/L). 3, 1
- Effects take 30-60 minutes to manifest 1
- Do NOT use in patients without metabolic acidosis—this is a common pitfall 1
- Promotes potassium excretion through increased distal sodium delivery 3, 1
Step 3: Remove Potassium from the Body
Loop diuretics (furosemide 40-80 mg IV) increase renal potassium excretion in patients with adequate kidney function. 1
Hemodialysis is the most reliable and effective method for potassium removal, especially in severe cases unresponsive to medical management, oliguria, or end-stage renal disease. 3, 1, 5, 4
Chronic Management (K+ 5.0-6.5 mEq/L)
Medication Review and Optimization
Eliminate or reduce contributing medications: NSAIDs, trimethoprim, heparin, beta-blockers, potassium supplements, salt substitutes. 1, 2
Do NOT discontinue RAAS inhibitors (ACE inhibitors, ARBs, mineralocorticoid antagonists) as these provide mortality benefit in cardiovascular and renal disease. 1
Potassium Binder Therapy (Preferred for Long-Term Management)
For K+ 5.0-6.5 mEq/L: Maintain RAAS inhibitor therapy at current dose and initiate approved potassium-lowering agent. 1, 2
Patiromer (Veltassa): Start at 8.4 g once daily, titrate up to 25.2 g daily based on potassium levels. 1
- Onset of action: ~7 hours 1
Sodium zirconium cyclosilicate (SZC/Lokelma): 10 g three times daily for 48 hours, then 5-15 g once daily for maintenance. 1
For K+ >6.5 mEq/L: Temporarily reduce or hold RAAS inhibitor and initiate potassium-lowering agent when levels >5.0 mEq/L. 1, 2
Avoid sodium polystyrene sulfonate (Kayexalate) due to delayed onset, limited efficacy, and risk of bowel necrosis. 1, 2
Diuretic Therapy
Loop or thiazide diuretics (furosemide 40-80 mg daily) promote urinary potassium excretion by stimulating flow to renal collecting ducts. 3, 1, 2
Fludrocortisone increases potassium excretion but carries significant risks of fluid retention, hypertension, and vascular injury—use cautiously. 3, 2
Monitoring Protocol
Check potassium within 1 week of starting or escalating RAAS inhibitors. 1, 2
Reassess 7-10 days after initiating potassium binder therapy or dose changes. 1, 2
High-risk patients require more frequent monitoring: those with chronic kidney disease, heart failure, diabetes, or history of hyperkalemia. 1, 2
For patients on potassium binders, monitor closely not only for efficacy but also to protect against hypokalemia, which may be even more dangerous than hyperkalemia. 1
Special Population: Chronic Kidney Disease
Maintain RAAS inhibitors aggressively in proteinuric CKD using potassium binders, as these drugs slow CKD progression. 1
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. 1
For CKD patients with K+ 6.2 mEq/L: Temporarily reduce or hold ACE inhibitor, then restart at lower dose with concurrent potassium binder therapy. 1
Key Pitfalls to Avoid
Do not rely solely on ECG findings—they are highly variable and less sensitive than laboratory tests. 1
Do not use sodium bicarbonate in patients without metabolic acidosis—it is only indicated when acidosis is present. 1
Ensure glucose is administered with insulin to prevent hypoglycemia. 1
Remember that calcium, insulin, and beta-agonists do not remove potassium from the body—they only temporize. 1
Maintain adequate hydration to support renal potassium excretion. 3
Team Approach
Optimal management involves cardiologists, nephrologists, primary care physicians, nurses, pharmacists, and dietitians working collaboratively. 3, 1, 2