Treatment of Hyperkalemia
For acute severe hyperkalemia (K+ ≥6.5 mEq/L or any ECG changes), immediately administer IV calcium gluconate 15-30 mL of 10% solution over 2-5 minutes to stabilize cardiac membranes, followed simultaneously by insulin 10 units with 50 mL of 50% dextrose IV and nebulized albuterol 20 mg to shift potassium intracellularly. 1, 2
Initial Assessment and Classification
Before initiating treatment, verify true hyperkalemia by excluding pseudohyperkalemia from hemolysis, repeated fist clenching, or poor phlebotomy technique—repeat the measurement with proper technique or use arterial sampling. 3, 2
Severity classification:
Obtain an 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 the absolute potassium level. 3, 1 However, do not rely solely on ECG findings as they are highly variable and less sensitive than laboratory values. 1, 2
Acute Management (K+ ≥6.5 mEq/L or ECG Changes)
Step 1: Cardiac Membrane Stabilization
Administer calcium gluconate 10% solution: 15-30 mL (1.5-3 grams) IV over 2-5 minutes, or calcium chloride 10%: 5-10 mL IV over 2-5 minutes. 3, 1, 2
Critical points about calcium:
- Effects begin within 1-3 minutes but last only 30-60 minutes 3, 1
- Calcium does NOT lower potassium—it only stabilizes cardiac membranes temporarily 3, 1
- Repeat dosing may be necessary if no ECG improvement within 5-10 minutes 3, 1
- Continuous cardiac monitoring is mandatory during and after administration 3, 1
Step 2: Shift Potassium Intracellularly
Administer all of the following simultaneously for maximum effect:
Insulin with glucose: 10 units regular insulin IV with 50 mL of 50% dextrose (or 25 grams glucose) 1, 2, 4
Sodium bicarbonate: 50 mEq IV over 5 minutes ONLY if metabolic acidosis is present (pH <7.35, bicarbonate <22 mEq/L) 1, 2
Step 3: Remove Potassium from the Body
For patients with adequate renal function:
For severe cases or renal failure:
- Hemodialysis is the most effective and reliable method for potassium removal, especially in patients with oliguria, end-stage renal disease, or those unresponsive to medical management 1, 2, 5
Chronic Management (K+ 5.0-6.5 mEq/L)
Medication Review and Adjustment
Eliminate or reduce contributing medications: 3, 1
- NSAIDs (attenuate diuretic effects and impair renal potassium excretion)
- Trimethoprim
- Heparin
- Potassium-sparing diuretics (spironolactone, amiloride, triamterene)
- Potassium supplements
- Salt substitutes (high potassium content)
For patients on RAAS inhibitors (ACE inhibitors, ARBs, mineralocorticoid antagonists):
- K+ 5.0-6.5 mEq/L: Maintain RAAS inhibitor at current dose and initiate approved potassium-lowering agent (patiromer or sodium zirconium cyclosilicate) 3, 1
- K+ >6.5 mEq/L: Temporarily reduce or hold RAAS inhibitor and initiate potassium-lowering agent 3, 1
- Do not permanently discontinue RAAS inhibitors in patients with cardiovascular disease, heart failure, or proteinuric CKD—these medications provide mortality benefit and slow disease progression 1
Potassium Binder Therapy
Sodium zirconium cyclosilicate (SZC/Lokelma): 1
- Dosing: 10 g three times daily for 48 hours, then 5-15 g once daily for maintenance
- Onset: ~1 hour (suitable for more urgent scenarios)
- Mechanism: Exchanges hydrogen and sodium for potassium
Patiromer (Veltassa): 1
- Dosing: Start 8.4 g once daily with food, titrate up to 25.2 g daily based on potassium levels
- Onset: ~7 hours
- Mechanism: Exchanges calcium for potassium in the colon
- Separate from other oral medications by at least 3 hours 1
- Monitor magnesium levels (causes hypomagnesemia) 1
Avoid sodium polystyrene sulfonate (Kayexalate): 3, 1
- Delayed onset, limited efficacy, and risk of bowel necrosis 3
- FDA label states it should NOT be used as emergency treatment for life-threatening hyperkalemia due to delayed onset 6
- Associated with intestinal necrosis, ischemic colitis, and perforation, especially with concomitant sorbitol use 6
Diuretic Optimization
Optimize loop or thiazide diuretics (furosemide 40-80 mg daily) to promote urinary potassium excretion if adequate renal function is present. 3, 1
Monitoring Protocol
- Check potassium within 1 week of starting or escalating RAAS inhibitors 3, 1, 2
- Reassess 7-10 days after initiating potassium binder therapy 3, 1
- After acute treatment with insulin/glucose, monitor potassium every 2-4 hours initially due to risk of rebound hyperkalemia 1
- High-risk patients require more frequent monitoring: those with chronic kidney disease, heart failure, diabetes, or history of hyperkalemia 3, 1, 2
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 1
- Never give insulin without glucose—hypoglycemia can be life-threatening 1, 2
- Never use sodium bicarbonate without documented metabolic acidosis—it is ineffective without acidosis 1, 2
- Remember that calcium, insulin, and beta-agonists do NOT remove potassium from the body—they only temporize, requiring definitive removal strategies 3, 1, 2
- Do not rely solely on ECG findings—they are highly variable and less sensitive than laboratory tests 1, 2
- Never administer calcium through the same IV line as sodium bicarbonate—precipitation will occur 1
Special Populations
Patients with advanced CKD (stage 4-5):
- Tolerate higher potassium levels (optimal range 3.3-5.5 mEq/L) due to compensatory mechanisms 1
- Maintain RAAS inhibitors aggressively using potassium binders, as these drugs slow CKD progression 1
- Target predialysis potassium of 4.0-5.5 mEq/L in hemodialysis patients to minimize mortality risk 1
Hemodialysis patients: