Hyperkalemia Management Guidelines

Classification and Severity Assessment

Hyperkalemia is classified as mild (5.0-5.9 mEq/L), moderate (6.0-6.4 mEq/L), or severe (≥6.5 mEq/L), with treatment urgency determined by both the absolute potassium level and the presence of ECG changes. 1

ECG changes (peaked T waves, flattened P waves, prolonged PR interval, widened QRS) indicate urgent treatment regardless of the potassium level 1
The rate of potassium rise matters as much as the absolute value—rapid increases are more dangerous than gradual elevations 2
Patients with atrioventricular heart block or other cardiac conduction abnormalities may develop symptoms at lower potassium levels than those without cardiac disease 2

Acute Life-Threatening Hyperkalemia (≥6.5 mEq/L or ECG Changes)

Step 1: Cardiac Membrane Stabilization (Immediate)

Administer IV calcium gluconate 15-30 mL of 10% solution over 2-5 minutes (or calcium chloride 5-10 mL of 10% solution) 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 stabilizes cardiac membranes temporarily 1
Repeat the dose after 5-10 minutes if ECG changes persist 1
Continuous cardiac monitoring is mandatory during administration 1

Critical pitfall: Never delay calcium administration while waiting for repeat lab confirmation if ECG changes are present 1

Step 2: Shift Potassium Intracellularly (Within 15-30 Minutes)

Give 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
Nebulized albuterol 10-20 mg in 4 mL: Onset 15-30 minutes, duration 2-4 hours 1
Sodium bicarbonate 50 mEq IV over 5 minutes ONLY if metabolic acidosis present (pH <7.35, bicarbonate <22 mEq/L): Onset 30-60 minutes 1

Critical pitfall: Never give insulin without glucose—hypoglycemia can be life-threatening 1

Critical pitfall: Never use sodium bicarbonate 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): For patients with adequate kidney function (eGFR >30 mL/min) 1
Hemodialysis: Most effective and reliable method for severe hyperkalemia, especially in renal failure, oliguria, or cases unresponsive to medical management 1
Potassium binders (patiromer or sodium zirconium cyclosilicate): For subacute management after stabilization, NOT for emergency treatment 3, 4

Step 4: Medication Review During Acute Episode

Temporarily discontinue or reduce at potassium ≥6.5 mEq/L: 1

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

Moderate Hyperkalemia (6.0-6.4 mEq/L, No ECG Changes)

Treat with insulin/glucose and albuterol to shift potassium into cells, and initiate potassium removal strategies. 1

Insulin 10 units regular IV + 25g dextrose 1
Nebulized albuterol 10-20 mg in 4 mL 1
Loop diuretics (furosemide 40-80 mg IV) if adequate renal function 1
Initiate potassium binder therapy:
- Sodium zirconium cyclosilicate (SZC/Lokelma): 10g three times daily for 48 hours, then 5-15g once daily for maintenance; onset ~1 hour 1
- Patiromer (Veltassa): 8.4g once daily with food, titrated up to 25.2g daily; onset ~7 hours 1

Do NOT give calcium unless ECG changes develop 1

Mild Hyperkalemia (5.0-5.9 mEq/L)

For Patients on RAAS Inhibitors with Cardiovascular Disease or Proteinuric CKD

Maintain RAAS inhibitors using potassium binders rather than discontinuing these life-saving medications. 1

Initiate patiromer or SZC while continuing RAAS inhibitor therapy 1
Review and eliminate contributing medications: NSAIDs, trimethoprim, heparin, beta-blockers, potassium supplements, salt substitutes 1
Optimize diuretic therapy: Loop or thiazide diuretics to increase urinary potassium excretion if adequate renal function present 1

Monitoring Protocol

Check potassium within 1 week of starting or escalating RAAS inhibitors, then reassess 7-10 days after initiating potassium binder therapy. 1

Individualize monitoring frequency based on CKD stage, heart failure, diabetes, or history of hyperkalemia 1
High-risk patients (CKD, diabetes, heart failure, history of hyperkalemia) require more frequent monitoring 2

Chronic Hyperkalemia Management

Potassium Binder Selection

Patiromer and sodium zirconium cyclosilicate are preferred over sodium polystyrene sulfonate (Kayexalate) for long-term management. 1

Sodium polystyrene sulfonate has significant limitations: Delayed onset of action, risk of bowel necrosis, and should be avoided for acute management 1
Patiromer: Binds potassium in exchange for calcium in the colon; starting dose 8.4g once daily, separated from other medications by at least 3 hours 1
SZC: Exchanges sodium and hydrogen for potassium; starting dose 10g three times daily for 48 hours, then 5-15g once daily; faster onset (~1 hour) 1

RAAS Inhibitor Management Algorithm

For patients with potassium 5.0-6.5 mEq/L on RAAS inhibitors: 1

Initiate approved potassium-lowering agent (patiromer or SZC)
Maintain RAAS inhibitor therapy unless alternative treatable cause identified
Do NOT permanently discontinue RAAS inhibitors—they provide mortality benefit in cardiovascular and renal disease

For patients with potassium >6.5 mEq/L on RAAS inhibitors: 1

Discontinue or reduce RAAS inhibitor temporarily
Initiate potassium-lowering agent when potassium >5.0 mEq/L
Restart RAAS inhibitor at lower dose once potassium <5.5 mEq/L with concurrent potassium binder therapy

Special Populations

Chronic Kidney Disease (Stage 4-5)

Patients with advanced CKD tolerate higher potassium levels (3.3-5.5 mEq/L for stage 4-5 CKD) due to compensatory mechanisms, but maintaining target potassium 4.0-5.0 mEq/L minimizes mortality risk. 1

Maintain RAAS inhibitors aggressively in proteinuric CKD using potassium binders, as these drugs slow CKD progression 1
Loop diuretics should be titrated to maintain euvolemia, not primarily for potassium management 1

Hemodialysis Patients

Target predialysis potassium of 4.0-5.5 mEq/L to minimize mortality risk. 1

Sodium zirconium cyclosilicate: 5g once daily on non-dialysis days, adjusted weekly in 5g increments 1
Patiromer: 8.4g once daily with food, titrated up to 16.8g or 25.2g daily based on response 1
Monitor magnesium levels in patients on patiromer to detect hypomagnesemia 1
Consider adjusting dialysate potassium concentration (typically 2.0-3.0 mEq/L) based on predialysis levels 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

Stringent dietary potassium restrictions may not be necessary in patients receiving potassium binder therapy 2
Avoid salt substitutes containing potassium, as they can exacerbate hyperkalemia 1

Critical Pitfalls to Avoid

Do not rely solely on ECG findings—they are highly variable and less sensitive than laboratory tests 1
Remember that calcium, insulin, and beta-agonists do NOT remove potassium from the body—they only temporize 1
Never delay treatment while waiting for repeat lab confirmation if ECG changes are present 1
Do not permanently discontinue RAAS inhibitors in patients with cardiovascular disease or proteinuric CKD—use potassium binders to maintain these life-saving medications 1
Ensure glucose is administered with insulin to prevent hypoglycemia 1

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