Hyperkalemia Management

Immediate Assessment and Risk Stratification

For any patient with hyperkalemia, immediately obtain an ECG and verify the result is not pseudohyperkalemia from hemolysis, repeated fist clenching, or poor phlebotomy technique before initiating treatment. 1

Classify severity: mild (5.0-5.9 mEq/L), moderate (6.0-6.4 mEq/L), or severe (≥6.5 mEq/L) 1
ECG changes (peaked T waves, flattened P waves, prolonged PR interval, widened QRS) mandate urgent treatment regardless of the potassium level 1
ECG findings are highly variable and less sensitive than laboratory tests, but their presence indicates immediate cardiac risk 1

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

Step 1: Cardiac Membrane Stabilization (First Priority)

Administer intravenous calcium gluconate 10% solution: 15-30 mL (1.5-3 grams) IV over 2-5 minutes immediately if potassium >6.5 mEq/L OR any ECG changes are present. 1

Effects begin within 1-3 minutes but last only 30-60 minutes 1
Calcium does NOT lower potassium—it only temporarily stabilizes cardiac membranes 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
Never administer calcium through the same IV line as sodium bicarbonate—precipitation will occur 1

Step 2: Shift Potassium Intracellularly (Simultaneous with Step 1)

Administer all three agents together for maximum effect: 1

Insulin 10 units regular IV + 25g dextrose (D50W): onset 15-30 minutes, duration 4-6 hours 1
- Verify potassium is not below 3.3 mEq/L before administering insulin 1
- Monitor glucose closely—hypoglycemia can be life-threatening 1
- Patients with low baseline glucose, no diabetes, female sex, and altered renal function are at higher risk of hypoglycemia 1
Nebulized albuterol 10-20 mg in 4 mL: onset 15-30 minutes, duration 2-4 hours 1
- Use as adjunctive therapy to augment insulin effects 1
Sodium bicarbonate 50 mEq IV over 5 minutes ONLY if metabolic acidosis present (pH <7.35, bicarbonate <22 mEq/L) 1
- Effects take 30-60 minutes to manifest 1
- Do not use without metabolic acidosis—it is ineffective and wastes time 1

Step 3: Remove Potassium from the Body (Definitive Treatment)

Choose based on renal function and clinical context: 1

Loop diuretics (furosemide 40-80 mg IV): if adequate kidney function exists 1
- Increases renal potassium excretion by stimulating flow to renal collecting ducts 1
Hemodialysis: most effective and reliable method for severe hyperkalemia 1, 2
- Reserved for severe cases unresponsive to medical management, oliguria, or end-stage renal disease 1
- Potassium levels can rebound as intracellular potassium redistributes—monitor every 2-4 hours initially post-dialysis 1

Step 4: Medication Review During Acute Episode

Temporarily discontinue or reduce these medications at K+ ≥6.5 mEq/L: 1

RAAS inhibitors (ACE inhibitors, ARBs, mineralocorticoid antagonists) 1
NSAIDs 1
Potassium-sparing diuretics (spironolactone, amiloride, triamterene) 1
Trimethoprim 1
Heparin 1
Beta-blockers 1
Potassium supplements and salt substitutes 1

Chronic Hyperkalemia Management (K+ 5.0-6.5 mEq/L)

Medication Optimization Strategy

For patients on RAAS inhibitors with K+ 5.0-6.5 mEq/L: maintain RAAS inhibitor therapy at current dose and initiate an approved potassium-lowering agent (patiromer or sodium zirconium cyclosilicate). 1

Do NOT permanently discontinue RAAS inhibitors—they provide mortality benefit in cardiovascular and renal disease 1
Once potassium <5.5 mEq/L, restart RAAS inhibitors at a lower dose with concurrent potassium binder therapy 1

Potassium Binder Selection

First-line: Sodium Zirconium Cyclosilicate (SZC/Lokelma) 1

Dosing: 10g three times daily for 48 hours, then 5-15g once daily for maintenance 1
Onset of action: approximately 1 hour 1
Mechanism: exchanges hydrogen and sodium for potassium 1
Monitor for edema due to sodium content 1

Second-line: Patiromer (Veltassa) 1

Dosing: 8.4g once daily with food, titrated up to 25.2g daily based on potassium levels 1
Onset of action: approximately 7 hours 1
Mechanism: exchanges calcium for potassium in the colon 1
Separate from other oral medications by at least 3 hours 1
Monitor magnesium levels—causes hypomagnesemia 1

Avoid: Sodium Polystyrene Sulfonate (Kayexalate) 1

Significant limitations: delayed onset, variable efficacy, risk of bowel necrosis 1
Should be avoided for acute management 1

Additional Chronic Management Strategies

Optimize loop or thiazide diuretics (furosemide 40-80 mg daily) to promote urinary potassium excretion if adequate renal function present 1
Eliminate contributing medications: NSAIDs, trimethoprim, heparin, beta-blockers, potassium supplements, salt substitutes 1
Fludrocortisone: increases potassium excretion but carries risks of fluid retention, hypertension, and vascular injury—use cautiously and only when other options are exhausted 1

Monitoring Protocol

Check potassium within 1 week of starting or escalating RAAS inhibitors 1

Reassess 7-10 days after initiating potassium binder therapy 1
High-risk patients (CKD, heart failure, diabetes, history of hyperkalemia) require more frequent monitoring 1
For patients on potassium binders, monitor closely for both efficacy and hypokalemia—hypokalemia may be even more dangerous than hyperkalemia 1

Special Population Considerations

Chronic Kidney Disease (CKD)

Maintain RAAS inhibitors aggressively in proteinuric CKD using potassium binders—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
Target predialysis potassium of 4.0-5.5 mEq/L to minimize mortality risk 1

Hemodialysis Patients

Start with SZC 5g once daily on non-dialysis days, adjust weekly in 5g increments based on predialysis potassium 1
Consider adjusting dialysate potassium concentration (typically 2.0-3.0 mEq/L) based on predialysis levels 1
Lower dialysate potassium (2.0 mEq/L) may be needed for recurrent severe hyperkalemia, but monitor for intradialytic arrhythmias 1

Cardiovascular Disease

Patients with cardiovascular disease on RAAS inhibitors require careful monitoring of potassium levels, with assessment 7-10 days after starting or increasing doses 1
Do not discontinue RAAS inhibitors—use potassium binders to enable continuation of these life-saving medications 1

Dietary Considerations

Evidence linking dietary potassium intake to serum potassium is limited, and a potassium-rich diet has multiple health benefits, including blood pressure reduction. 1

Newer potassium binders may allow for less restrictive dietary potassium restrictions 1
Focus on reducing intake of nonplant sources of potassium rather than stringent restriction of all potassium-rich foods 3
Avoid "low-salt" substitutes—they have high potassium content 1

Critical Pitfalls to Avoid

Never delay treatment while waiting for repeat lab confirmation if ECG changes are present—ECG changes indicate urgent need regardless of the exact potassium value. 1

Never give insulin without glucose—hypoglycemia can be life-threatening 1
Never use sodium bicarbonate without metabolic acidosis—it is ineffective and wastes time 1
Remember that calcium, insulin, and beta-agonists are temporizing measures only—they do NOT remove potassium from the body 1
Do not rely solely on ECG findings—they are highly variable and less sensitive than laboratory tests 1
Failure to initiate concurrent potassium-lowering therapies will result in recurrent life-threatening arrhythmias within 30-60 minutes after calcium administration 1

Team Approach

Optimal management involves a multidisciplinary team including cardiologists, nephrologists, primary care physicians, nurses, pharmacists, social workers, and dietitians working collaboratively. 1

What are the management strategies for hyperkalemia?

Help us tailor your experience