What are the management strategies for hyperkalemia and hypokalemia?

Potassium Management: Hyperkalemia and Hypokalemia

Hyperkalemia Management

For acute hyperkalemia with potassium ≥6.5 mEq/L or any ECG changes, immediately administer IV calcium gluconate 15-30 mL over 2-5 minutes for cardiac membrane stabilization, followed by insulin 10 units with dextrose and nebulized albuterol 20 mg to shift potassium intracellularly. 1, 2

Initial Assessment and Classification

Before initiating treatment, verify the result is not pseudohyperkalemia from hemolysis, repeated fist clenching, or poor phlebotomy technique by repeating the measurement with proper technique or arterial sampling 1, 2. Severity classification guides management:

• Mild: 5.0-5.9 mEq/L 1
• Moderate: 6.0-6.4 mEq/L 1
• Severe: ≥6.5 mEq/L 1

Critical pitfall: Do not rely solely on ECG findings—they are highly variable and less sensitive than laboratory tests, though peaked T waves, flattened P waves, prolonged PR interval, and widened QRS complexes indicate urgent treatment regardless of potassium level 1, 2.

Acute Hyperkalemia Treatment Algorithm

Step 1: Cardiac Membrane Stabilization (Immediate)

Administer IV calcium if potassium >6.5 mEq/L or any ECG changes are present 2:

• Calcium gluconate (10%): 15-30 mL IV over 2-5 minutes 1, 2
• Calcium chloride (10%): 5-10 mL IV over 2-5 minutes (use in cardiac arrest) 1, 3
• Effects begin within 1-3 minutes but are temporary (30-60 minutes) and do not reduce serum potassium 1

Important caveat: In patients with malignant hyperthermia and hyperkalemia, calcium should only be used in extremis as it may contribute to calcium overload of the myoplasm 1.

Step 2: Intracellular Potassium Shift (Within 15-30 minutes)

Insulin with glucose (onset 15-30 minutes, duration 4-6 hours) 1, 2:

• Standard dose: 10 units regular insulin IV 1
• Alternative dosing to reduce hypoglycemia risk: 5 units or 0.1 units/kg 1, 4
• Administer with 50 mL of 50% dextrose (25 g) or 50 g dextrose for higher-risk patients 3, 4
• Critical safety measure: Verify potassium is not below 3.3 mEq/L before administering insulin 1
• Monitor glucose hourly for at least 4-6 hours after administration to prevent hypoglycemia 1, 4
• Patients at higher risk for hypoglycemia: low baseline glucose, no diabetes history, female sex, altered renal function 1, 4

Beta-agonists (onset 15-30 minutes, duration 2-4 hours) 1:

• Nebulized albuterol 20 mg in 4 mL as adjunctive therapy 1, 2

Sodium bicarbonate (onset 30-60 minutes) 1:

• Use ONLY in patients with concurrent metabolic acidosis (pH <7.35, bicarbonate <22 mEq/L) 1, 2
• Do not use in patients without metabolic acidosis—this is a common error 1, 2
• Promotes potassium excretion through increased distal sodium delivery 1

Key principle: Remember that calcium, insulin, and beta-agonists do not remove potassium from the body—they only temporize 1, 2.

Step 3: Potassium Removal from Body

Loop diuretics (for patients with adequate kidney function) 1:

• Furosemide 40-80 mg IV to increase renal potassium excretion 1

Hemodialysis (most effective method) 1, 2:

• Use for severe hyperkalemia unresponsive to medical management, oliguria, or end-stage renal disease 1, 5
• Most reliable and effective method for potassium removal 1, 6

Potassium binders (avoid sodium polystyrene sulfonate) 1:

• Sodium polystyrene sulfonate (Kayexalate) has significant limitations, including delayed onset and risk of bowel necrosis—avoid for acute management 1, 7

Chronic Hyperkalemia Management

For patients on RAAS inhibitors with potassium 5.0-6.5 mEq/L, initiate an approved potassium-lowering agent (patiromer or sodium zirconium cyclosilicate) and maintain RAAS inhibitor therapy—do not discontinue these life-saving medications. 1, 2

Medication Review and Optimization

Eliminate or reduce contributing medications 1, 2:

• NSAIDs, trimethoprim, heparin, beta-blockers, potassium supplements, salt substitutes 1
• Do NOT discontinue RAAS inhibitors (ACE inhibitors, ARBs, mineralocorticoid antagonists) as these provide mortality benefit in cardiovascular and renal disease 1

RAAS Inhibitor Management Algorithm

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

• Initiate approved potassium-lowering agent (patiromer or SZC) 1
• Maintain RAAS inhibitor therapy unless alternative treatable cause identified 1

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

• Discontinue or reduce RAAS inhibitor temporarily 1
• Initiate potassium-lowering agent when levels >5.0 mEq/L 1
• Monitor potassium closely 1

Potassium Binder Therapy (Preferred for Long-term Management)

Patiromer (Veltassa) 1, 2:

• Starting dose: 8.4 g once daily, titrated up to 25.2 g daily based on potassium levels 1
• Onset of action: ~7 hours 1

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

• Acute phase: 10 g three times daily for 48 hours 1
• Maintenance: 5-15 g once daily 1
• Onset of action: ~1 hour (effective for acute hyperkalemia ≥5.8 mEq/L) 1

Diuretic Therapy

Loop or thiazide diuretics promote urinary potassium excretion by stimulating flow to renal collecting ducts 1, 8:

• Furosemide 40-80 mg daily if adequate renal function present 1

Fludrocortisone increases potassium excretion but carries risks of fluid retention, hypertension, and vascular injury—use with caution 1, 8.

Monitoring Protocol

Check potassium within 1 week of starting or escalating RAAS inhibitors 1, 2:

• Reassess 7-10 days after starting or increasing RAAS inhibitor doses 1, 2
• Reassess 7-10 days after initiating potassium binder therapy 1

High-risk patients require more frequent monitoring 1, 2:

• Chronic kidney disease, heart failure, diabetes mellitus, or history of hyperkalemia 1, 2
• Optimal potassium range 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

Special Populations

Patients with CKD and proteinuria 1:

• Maintain RAAS inhibitors aggressively using potassium binders, as these drugs slow CKD progression 1

Patients with cardiovascular disease 1:

• High "normal" potassium concentrations (>5.0 mEq/L) may be associated with adverse outcomes in heart failure, hypertension, or CKD 1
• Focus on hyperkalemia with clinical impact and rapid fluctuations rather than arbitrary thresholds alone 1

Dietary Considerations

Evidence linking dietary potassium intake to serum potassium is limited 1:

• A potassium-rich diet has multiple health benefits, including blood pressure reduction 1
• Dietary restriction should be approached cautiously in otherwise healthy individuals 1
• Focus on reducing nonplant sources of potassium rather than blanket restriction 6
• Avoid potassium supplements and salt substitutes in patients with hyperkalemia 1

Management of Mild Hyperkalemia (5.0-5.5 mEq/L)

Do not initiate acute interventions (calcium, insulin, or albuterol) for mild hyperkalemia without ECG changes or symptoms 1:

• Consider loop diuretics to enhance urinary potassium excretion in patients with adequate renal function 1
• Carefully evaluate potassium-sparing medications 1

Hypokalemia Management

For hypokalemia treatment, potassium chloride supplementation should be reserved for patients who cannot tolerate or refuse liquid/effervescent preparations, or when compliance is an issue. 3

Indications for Potassium Supplementation

Potassium chloride is indicated for 3:

• Treatment of hypokalemia with or without metabolic alkalosis 3
• Digitalis intoxication 3
• Hypokalemic familial periodic paralysis 3
• Prevention of hypokalemia in high-risk patients (digitalized patients or those with significant cardiac arrhythmias) 3

Treatment Approach

If hypokalemia results from diuretic therapy 3:

• Consider using a lower dose of diuretic, which may be sufficient without leading to hypokalemia 3
• Check serum potassium periodically 3
• If hypokalemia occurs, dietary supplementation with potassium-containing foods may be adequate for milder cases 3
• In more severe cases, or if diuretic dose adjustment is ineffective or unwarranted, supplementation with potassium salts may be indicated 3

For uncomplicated essential hypertension 3:

• Potassium supplementation is often unnecessary when patients have a normal dietary pattern and low doses of diuretics are used 3

Safety Considerations

The administration of oral potassium salts to persons with normal excretory mechanisms rarely causes serious hyperkalemia 3. However, if excretory mechanisms are impaired or potassium is administered too rapidly intravenously, potentially fatal hyperkalemia can result 3.