What is the appropriate management of hyperkalemia?

Treatment of Hyperkalemia

For severe hyperkalemia (≥6.5 mEq/L) or any ECG changes, immediately administer IV calcium gluconate 10% (15–30 mL over 2–5 minutes) to stabilize the cardiac membrane, followed simultaneously by insulin 10 units IV with 25g dextrose and nebulized albuterol 10–20 mg to shift potassium intracellularly, then initiate definitive potassium removal with hemodialysis or loop diuretics depending on renal function. 1, 2

Initial Assessment

Obtain a 12-lead ECG immediately for every patient with suspected hyperkalemia, as peaked T waves, flattened P waves, prolonged PR interval, or widened QRS mandates urgent treatment even when potassium is only mildly elevated. 2

• Verify the result is not pseudohyperkalemia from hemolysis, fist clenching, or poor phlebotomy technique before initiating aggressive treatment. 1, 2
• ECG findings are less sensitive than laboratory values and should not replace serum potassium measurement. 1, 2
• Plasma potassium values are typically 0.1–0.4 mEq/L lower than serum values due to platelet potassium release during clotting. 2

Severity Classification

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

Acute Hyperkalemia Management

Step 1: Cardiac Membrane Stabilization (Immediate)

Administer IV calcium gluconate 10% (15–30 mL over 2–5 minutes) for any ECG changes OR serum potassium ≥6.5 mEq/L. 1, 2

• Alternatively, use calcium chloride 10% (5–10 mL over 2–5 minutes) when central venous access is available. 1, 2
• Onset of action: 1–3 minutes; duration: 30–60 minutes. 1, 2
• Critical caveat: Calcium does NOT lower potassium—it only stabilizes cardiac membranes temporarily. 1, 2
• Repeat the same dose if no ECG improvement within 5–10 minutes. 1, 2
• Continuous cardiac monitoring is mandatory during and after administration. 1
• Never delay calcium administration while awaiting repeat potassium levels when ECG changes are present. 1, 2

Step 2: Intracellular Potassium Shift (Administer Simultaneously)

Insulin-Glucose Therapy

Give 10 units regular insulin IV push with 25g dextrose (50 mL D50W). 1, 2

• Reduces serum potassium by 0.5–1.2 mEq/L within 30–60 minutes. 1, 2
• Duration: 4–6 hours. 1, 2
• Never give insulin without glucose—hypoglycemia can be fatal. 1, 2
• Monitor blood glucose every 30–60 minutes after administration. 2
• Patients with low baseline glucose, no diabetes, female sex, or impaired renal function are at higher risk of hypoglycemia. 1
• Can be repeated every 4–6 hours as needed, carefully monitoring glucose and potassium levels. 1

Beta-Agonist Therapy

Administer nebulized albuterol 10–20 mg in 4 mL over 10–15 minutes. 1, 2

• Lowers potassium by 0.5–1.0 mEq/L within 30 minutes. 1, 2
• Duration: 2–4 hours. 1, 2
• Can be repeated every 2 hours if needed. 1, 2
• Combined insulin-glucose plus albuterol is more effective than either alone. 1, 2

Sodium Bicarbonate (ONLY with Metabolic Acidosis)

Administer 50 mEq IV over 5 minutes ONLY when pH <7.35 AND bicarbonate <22 mEq/L. 1, 2

• Onset: 30–60 minutes. 1, 2
• Promotes potassium excretion through increased distal sodium delivery and counters acidosis-induced potassium release. 1, 2
• Do NOT use without documented metabolic acidosis—it is ineffective and wastes time. 1, 2

Step 3: Definitive Potassium Removal

Hemodialysis (Most Reliable Method)

Hemodialysis is the most effective and reliable method for severe hyperkalemia. 1, 2, 3, 4

Absolute indications: 1, 2

• Serum potassium >6.5 mEq/L unresponsive to medical therapy
• Oliguria or anuria
• End-stage renal disease
• Severe renal impairment (eGFR <15 mL/min)
• Ongoing potassium release (tumor lysis syndrome, rhabdomyolysis)
• Persistent ECG changes despite medical management

In hemodynamically unstable patients (hypotensive, requiring vasopressors), continuous renal replacement therapy (CRRT) is preferred over intermittent hemodialysis to minimize rapid fluid shifts and reduce intradialytic hypotension risk. 1

Loop Diuretics

Administer furosemide 40–80 mg IV to increase renal potassium excretion in patients with adequate kidney function. 1, 2

• Effective only when eGFR >30 mL/min and patient is non-oliguric. 1, 2
• Titrate to maintain euvolemia, not primarily for potassium management. 1

Chronic Hyperkalemia Management

Medication Review and Adjustment

Review and eliminate or reduce contributing medications: 1, 2, 3

• NSAIDs
• Trimethoprim-containing agents
• Heparin
• Beta-blockers
• Potassium-sparing diuretics (spironolactone, amiloride, triamterene)
• Potassium supplements and salt substitutes

RAAS Inhibitor Management

Do NOT permanently discontinue RAAS inhibitors (ACE inhibitors, ARBs, mineralocorticoid receptor antagonists) in patients with cardiovascular disease, heart failure, or proteinuric CKD—these provide mortality benefit and slow disease progression. 1, 2, 3

Algorithm for RAAS inhibitor management: 1, 2

• Potassium 5.0–6.5 mEq/L: Maintain RAAS inhibitor at current dose and initiate potassium binder (patiromer or sodium zirconium cyclosilicate).
• Potassium >6.5 mEq/L: Temporarily hold or reduce RAAS inhibitor dose; initiate potassium binder once potassium <5.0 mEq/L, then restart RAAS inhibitor at lower dose with concurrent binder therapy.
• Check potassium within 1 week of starting or escalating RAAS inhibitors. 1, 2
• Reassess potassium 7–10 days after dose changes. 1

Potassium Binders

Sodium Zirconium Cyclosilicate (SZC/Lokelma)

Preferred for urgent scenarios due to rapid onset. 1, 2

• Dosing: 10g three times daily for 48 hours, then 5–15g once daily for maintenance. 1, 2
• Onset: ~1 hour. 1, 2
• Reduces serum potassium within 1 hour of a single 10g dose. 1
• FDA indication: Treatment of hyperkalemia in adults; NOT for emergency treatment of life-threatening hyperkalemia due to delayed onset. 5
• Monitor for edema due to sodium content. 1

Patiromer (Veltassa)

Preferred for chronic management. 1, 2

• Dosing: 8.4g once daily with food, titrated up to 25.2g daily based on potassium response. 1, 2
• Onset: ~7 hours. 1, 2
• Must be separated from other oral medications by at least 3 hours to avoid reduced absorption. 1
• Monitor magnesium levels—patiromer causes hypomagnesemia. 1
• Mechanism: Exchanges calcium for potassium in the colon. 1

Sodium Polystyrene Sulfonate (Kayexalate)

AVOID due to serious safety concerns. 1, 2

• Associated with bowel necrosis, colonic ischemia, and doubling of risk for serious gastrointestinal adverse events. 1
• Variable and inconsistent onset of action with limited efficacy data. 1
• FDA indication: Treatment of hyperkalemia; should NOT be used as emergency treatment due to delayed onset. 6

Dietary Considerations

Evidence linking dietary potassium intake to serum levels is limited. 1, 2

• Potassium-rich diets provide cardiovascular benefits including blood pressure reduction. 1
• Focus dietary restriction on reducing nonplant sources of potassium rather than stringent overall restriction. 1, 7
• Eliminate high-potassium salt substitutes. 1
• Newer potassium binders may allow less restrictive dietary potassium restrictions. 1

Special Populations

Chronic Kidney Disease (Stage 4–5)

Maintain RAAS inhibitors aggressively using potassium binders, as these drugs slow CKD progression. 1, 2

• Target potassium: 4.0–5.0 mEq/L to minimize mortality risk. 1
• Broader optimal range: 3.3–5.5 mEq/L for stage 4–5 CKD. 1, 2
• Patients with advanced CKD tolerate higher potassium levels due to compensatory mechanisms. 1

Hemodialysis Patients

Target predialysis potassium: 4.0–5.5 mEq/L. 1, 3

• First-line agent: Sodium zirconium cyclosilicate 5g once daily on non-dialysis days, adjusted weekly in 5g increments. 1, 3
• Second-line agent: Patiromer 8.4g once daily with food, separated from other medications by ≥3 hours. 1
• Adjust 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

Heart Failure Patients

Target potassium: 4.0–5.0 mEq/L, as both hypo- and hyperkalemia increase mortality. 1, 2

• Continue RAAS inhibitors and aldosterone antagonists with binder support. 1
• SGLT2 inhibitors may reduce hyperkalemia risk. 1
• Patiromer enables 86% of patients to remain on spironolactone 50mg daily versus 66% with placebo. 1

Monitoring Protocol

Acute Phase

• Re-measure serum potassium 1–2 hours after insulin-glucose or beta-agonist therapy. 2
• Continue potassium checks every 2–4 hours until stable. 1, 2
• Obtain repeat ECG to confirm resolution of cardiac changes. 2
• Monitor blood glucose every 30–60 minutes after insulin administration. 2

Post-Acute Phase

• Check potassium within 1 week of starting or escalating RAAS inhibitors. 1, 2
• Reassess 7–10 days after initiating potassium binder therapy. 1, 2
• Individualize monitoring frequency based on eGFR, heart failure, diabetes, or history of hyperkalemia. 1, 2

Critical Pitfalls to Avoid

• Do NOT delay calcium administration while awaiting repeat potassium levels when ECG changes are present—ECG changes indicate urgent need regardless of exact potassium value. 1, 2
• Never give insulin without glucose—hypoglycemia can be fatal. 1, 2
• Recognize that calcium, insulin, and beta-agonists are temporizing measures only—they do NOT remove potassium from the body. 1, 2
• Do NOT use sodium bicarbonate without documented metabolic acidosis—it is ineffective without acidosis. 1, 2
• Do NOT permanently discontinue RAAS inhibitors—use potassium binders to maintain these life-saving medications. 1, 2, 3
• Do NOT rely solely on ECG findings—they are highly variable and less sensitive than laboratory tests. 1, 2
• Do NOT use sodium polystyrene sulfonate (Kayexalate)—risk of bowel necrosis outweighs limited efficacy. 1, 2