Management of Hyperkalemia

Severity Classification and Initial Assessment

Hyperkalemia should be classified as mild (>5.0 to <5.5 mEq/L), moderate (5.5 to 6.0 mEq/L), or severe (>6.0 mEq/L), with immediate ECG assessment mandatory for all patients to guide treatment urgency. 1, 2

Obtain an ECG immediately to assess for peaked T waves, flattened P waves, prolonged PR interval, or widened QRS complex—these findings mandate urgent treatment regardless of the exact potassium value 1, 3
Rule out pseudohyperkalemia by repeating the measurement with proper blood sampling technique, as hemolysis or tissue breakdown during phlebotomy can falsely elevate potassium levels 1, 3
Any hyperkalemia with ECG changes or potassium >6.0 mEq/L requires hospital admission due to high risk of cardiac arrhythmias and sudden death 1, 2

Common pitfall: ECG changes can be highly variable and less sensitive than laboratory values, but their presence indicates urgent need for treatment—never delay intervention while waiting for repeat laboratory confirmation if ECG changes are present 1, 3

Emergency Management of Severe Hyperkalemia (>6.0 mEq/L or ECG Changes)

For severe hyperkalemia or any ECG changes, administer intravenous calcium immediately for cardiac membrane stabilization, followed by agents to shift potassium intracellularly, then initiate potassium removal strategies. 1, 2, 3

Step 1: Cardiac Membrane Stabilization (Onset: 1-3 minutes, Duration: 30-60 minutes)

Administer calcium gluconate 10%: 15-30 mL (1.5-3 grams) IV over 2-5 minutes with continuous cardiac monitoring 1, 2, 3
Alternative: calcium chloride 10%: 5-10 mL IV over 2-5 minutes (preferred for central access) 1, 3
If no ECG improvement within 5-10 minutes, repeat the dose 3
Critical caveat: Calcium does NOT lower serum potassium—it only temporarily stabilizes cardiac membranes for 30-60 minutes 2, 3

Step 2: Shift Potassium Intracellularly (Onset: 15-30 minutes, Duration: 4-6 hours)

Administer all three agents together for maximum effect: 3

Insulin + glucose: Regular insulin 10 units IV with 25 grams dextrose (50 mL of 50% dextrose or 250 mL of 10% dextrose) 1, 2, 3
Nebulized albuterol: 10-20 mg in 4 mL nebulized over 10 minutes 1, 2, 3
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

Critical pitfall: Never give insulin without glucose—hypoglycemia can be life-threatening. Monitor glucose closely, especially in patients with low baseline glucose, no diabetes, female sex, or altered renal function 1, 3

Important note: Sodium bicarbonate should ONLY be used in patients with metabolic acidosis—it is ineffective without acidosis and wastes time 1, 2, 3

Step 3: Remove Potassium from the Body

Loop diuretics: Furosemide 40-80 mg IV if adequate renal function (eGFR >30 mL/min/1.73m²) 1, 2, 3
Hemodialysis: Most effective and reliable method for severe hyperkalemia, especially in patients with renal failure, oliguria, or unresponsive to medical management 1, 2, 3
Potassium binders: Initiate sodium zirconium cyclosilicate (SZC) 10 g three times daily for 48 hours (onset ~1 hour) or patiromer 8.4 g once daily (onset ~7 hours) 1, 2, 3

Step 4: Medication Review and Adjustment

Temporarily discontinue or reduce when potassium >6.5 mEq/L: 1, 2, 3

RAAS inhibitors (ACE inhibitors, ARBs, mineralocorticoid receptor antagonists)
NSAIDs
Potassium-sparing diuretics (spironolactone, amiloride, triamterene)
Trimethoprim, heparin, beta-blockers
Potassium supplements and salt substitutes

Management of Moderate Hyperkalemia (5.5-6.0 mEq/L)

For moderate hyperkalemia without ECG changes, focus on potassium removal strategies and medication adjustment rather than emergency temporizing measures. 1, 2

Obtain ECG immediately to confirm absence of cardiac effects 1
Restrict potassium intake to <3 grams per day (50-70 mmol/day) 1
Loop diuretics: Furosemide 40-80 mg daily if adequate renal function 1, 2, 3
Initiate potassium binder: Sodium zirconium cyclosilicate 10 g three times daily for 48 hours, then 5-15 g once daily for maintenance, OR patiromer 8.4 g once daily, titrated up to 25.2 g daily based on response 1, 2, 3
Review and adjust RAAS inhibitors: Reduce dose rather than discontinue, as these provide mortality benefit in heart failure and chronic kidney disease 1, 2, 3
Recheck potassium within 24-48 hours, then within 1 week 1

Critical decision point: If potassium rises above 6.0 mEq/L on repeat testing, immediate hospital referral is indicated 1

Management of Mild Hyperkalemia (>5.0 to <5.5 mEq/L)

For mild asymptomatic hyperkalemia with normal ECG, conservative management with medication review and dietary modification is appropriate without acute interventions. 1, 3

Confirm with repeat measurement to rule out pseudohyperkalemia 1
Obtain ECG to assess for cardiac effects 1
Review and potentially adjust medications contributing to hyperkalemia (RAAS inhibitors, NSAIDs, potassium-sparing diuretics) 1, 3
Counsel patients to avoid high-potassium foods: bananas, oranges, melons, potatoes, tomato products, salt substitutes, legumes, chocolate, yogurt 1
Consider loop diuretics if adequate kidney function 1
Recheck potassium within 1 week 1

Important note: Do not initiate acute interventions (calcium, insulin, albuterol) for mild hyperkalemia without ECG changes or symptoms 3

Chronic Hyperkalemia Management and Prevention of Recurrence

The priority in chronic hyperkalemia is maintaining beneficial RAAS inhibitor therapy using potassium binders rather than permanently discontinuing these life-saving medications. 1, 2, 3

Medication Management Algorithm

For patients on RAAS inhibitors: 1, 2, 3

Potassium 5.0-6.5 mEq/L: Initiate potassium binder (patiromer or SZC) while maintaining RAAS inhibitor therapy at current or reduced dose
Potassium >6.5 mEq/L: Temporarily discontinue or reduce RAAS inhibitor, initiate potassium binder, then restart RAAS inhibitor at lower dose once potassium <5.0 mEq/L

Potassium Binder Selection

Sodium zirconium cyclosilicate (SZC/Lokelma): 1, 2, 3

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
Monitoring: Watch for edema due to sodium content

Patiromer (Veltassa): 1, 2, 3

Dosing: 8.4 g once daily with food, titrated up to 25.2 g daily
Onset: ~7 hours
Mechanism: Exchanges calcium for potassium in the colon
Administration: Separate from other oral medications by at least 3 hours
Monitoring: Check magnesium levels (causes hypomagnesemia)

Avoid sodium polystyrene sulfonate (Kayexalate): Risk of bowel necrosis and serious gastrointestinal adverse events—should not be used chronically 1, 2, 3

Monitoring Protocol

Check potassium within 1 week of starting or escalating RAAS inhibitors 1, 2, 3
Reassess 7-10 days after initiating potassium binder therapy 1, 3
High-risk patients (CKD, heart failure, diabetes, history of hyperkalemia) require more frequent monitoring 1, 2, 3
Monitor for hypokalemia in patients on potassium binders, as this may be more dangerous than hyperkalemia 3

Dietary Modifications

Restrict potassium intake to <3 grams per day 1
Avoid high-potassium foods: bananas, oranges, potatoes, tomatoes, salt substitutes, legumes, chocolate, yogurt, certain herbal supplements 1
Emerging evidence: Direct links between dietary potassium and serum levels are limited; potassium-rich diets have cardiovascular benefits including blood pressure reduction—newer potassium binders may allow less restrictive dietary approaches 3

Special Population: Chronic Kidney Disease

Patients with CKD have a broader optimal potassium range (3.3-5.5 mEq/L for stage 4-5 CKD) and require aggressive maintenance of RAAS inhibitors using potassium binders, as these medications slow CKD progression. 2, 3

For CKD patients with potassium 5.5 mEq/L and eGFR 50 mL/min/1.73m², initiate potassium binder while continuing RAAS inhibitors at potentially reduced doses 1, 2
Loop diuretics remain effective at eGFR 50 mL/min/1.73m² for enhancing potassium excretion 1, 2
Target predialysis potassium of 4.0-5.5 mEq/L in dialysis patients to minimize mortality risk 3
Consider adjusting dialysate potassium concentration (typically 2.0-3.0 mEq/L) based on predialysis levels 3

Critical Pitfalls to Avoid

Never delay treatment of severe hyperkalemia while waiting for repeat laboratory values if ECG changes are present 1, 3
Never discontinue RAAS inhibitors permanently due to hyperkalemia—dose reduction plus potassium binders is preferred to maintain mortality and morbidity benefits 1, 2, 3
Never use sodium bicarbonate without metabolic acidosis—it is ineffective and wastes time 1, 2, 3
Never give insulin without glucose—hypoglycemia can be life-threatening 1, 3
Never rely solely on ECG findings—they are variable and less sensitive than laboratory tests, but their presence mandates urgent treatment 1, 3
Remember that calcium, insulin, and beta-agonists are temporizing measures only—they do NOT remove potassium from the body and must be followed by definitive elimination strategies 2, 3
Never use chronic sodium polystyrene sulfonate—risk of bowel necrosis and serious gastrointestinal complications 1, 2, 3
Do not overlook rebound hyperkalemia 2-4 hours after temporary measures wear off, especially post-dialysis or in tumor lysis syndrome 1, 3

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