How should acute hyperkalemia be managed, considering severity, ECG changes, and comorbidities such as renal failure, heart failure, or diabetes?

Hyperkalemia Treatment

For acute hyperkalemia ≥6.0 mEq/L or with 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 25 g dextrose and nebulized albuterol 10–20 mg to shift potassium intracellularly, then initiate definitive potassium removal with loop diuretics (if eGFR >30 mL/min), hemodialysis (if severe/refractory), or potassium binders (sodium zirconium cyclosilicate or patiromer) for subacute management. 1, 2

Immediate Assessment and Risk Stratification

• Obtain an ECG immediately in any patient with suspected hyperkalemia to detect life-threatening cardiac changes (peaked T waves, absent P waves, prolonged PR interval, widened QRS, sine-wave pattern) regardless of the measured serum potassium level. 1, 2
• Verify that elevated potassium is not pseudohyperkalemia from hemolysis, fist clenching, or poor phlebotomy technique by repeating the measurement with proper technique or arterial sampling. 1, 2
• Classify hyperkalemia severity: mild (5.0–5.9 mEq/L), moderate (6.0–6.4 mEq/L), or severe (≥6.5 mEq/L). 1, 2
• Do not delay treatment while awaiting repeat laboratory confirmation when ECG changes are present—urgent therapy is required regardless of exact potassium value. 1, 2

Acute Hyperkalemia Management (K⁺ ≥6.0 mEq/L or ECG Changes)

Step 1: Cardiac Membrane Stabilization (Does NOT Lower Potassium)

• Administer IV calcium gluconate 10% (15–30 mL) over 2–5 minutes immediately when ECG changes are present. 1, 2, 3, 4
• Onset of action is 1–3 minutes, but duration is only 30–60 minutes. 1, 2
• Calcium stabilizes the myocardium but does not remove potassium from the body. 1, 2
• Repeat the dose if ECG does not improve within 5–10 minutes. 1, 2
• Alternatively, use calcium chloride 10% (5–10 mL) IV over 2–5 minutes if central venous access is available, as it is more potent. 2

Step 2: Intracellular Potassium Shift (Temporizing Measures—Administer Simultaneously)

Insulin-Glucose Therapy

• Give insulin 10 units regular IV together with 25 g dextrose (D50W 50 mL). 1, 2, 4
• Expected potassium reduction: 0.5–1.2 mEq/L within 30–60 minutes. 1, 2
• Effect lasts 4–6 hours; rebound hyperkalemia commonly occurs after this period. 1, 2
• Never administer insulin without concomitant glucose, as this can precipitate severe hypoglycemia. 1, 2
• Monitor blood glucose closely after administration, especially in patients with low baseline glucose, no diabetes history, female sex, or altered renal function. 2

Beta-Agonist Therapy

• Administer nebulized albuterol 10–20 mg in 4 mL over 10–15 minutes. 1, 2, 4
• Expected potassium reduction: 0.5–1.0 mEq/L within 30 minutes. 1, 2
• Duration of effect: 2–4 hours. 1, 2
• Can be repeated every 2 hours if needed. 2
• The combined insulin-glucose plus albuterol regimen is more effective than either modality alone. 2

Sodium Bicarbonate (ONLY with Metabolic Acidosis)

• Administer sodium bicarbonate 50 mEq IV over 5 minutes ONLY if metabolic acidosis is present (pH <7.35, bicarbonate <22 mEq/L). 1, 2, 4
• Onset of action: 30–60 minutes. 1, 2
• Do not use sodium bicarbonate without documented metabolic acidosis—it is ineffective and wastes time. 1, 2

Step 3: Definitive Potassium Removal

Loop Diuretics (Renal Function Dependent)

• Use loop diuretics (e.g., furosemide 40–80 mg IV) when renal function is adequate (eGFR >30 mL/min) to promote urinary potassium excretion. 1, 2
• Effective only in non-oliguric patients with preserved kidney function. 2

Hemodialysis (Most Reliable Method)

• Hemodialysis is the most reliable and effective method for severe hyperkalemia, especially in patients with oliguria, end-stage renal disease, or refractory hyperkalemia despite medical measures. 1, 2, 4, 5, 6
• Absolute indications for dialysis include:
  • Serum potassium >6.5 mEq/L unresponsive to medical therapy 2
  • Oliguria or anuria 2
  • End-stage renal disease 2
  • Ongoing potassium release (e.g., tumor lysis syndrome, rhabdomyolysis) 2
  • Severe renal impairment (eGFR <15 mL/min) 2
  • Persistent ECG changes despite medical management 2
• In hemodynamically unstable patients, continuous renal replacement therapy (CRRT) is preferred over intermittent hemodialysis to minimize rapid fluid shifts and reduce intradialytic hypotension risk. 2

Potassium Binders (Subacute Management)

• Initiate sodium zirconium cyclosilicate (SZC/Lokelma) 10 g three times daily for 48 hours, then 5–15 g once daily for maintenance. 1, 2, 5, 6

  • Onset of action: approximately 1 hour. 1, 2
  • Reduces serum potassium within 1 hour of a single 10-g dose. 2
  • Suitable for more urgent outpatient scenarios. 2

• Initiate patiromer (Veltassa) 8.4 g once daily with food, titrating up to 25.2 g daily based on potassium levels. 1, 2, 5, 6

  • Onset of action: approximately 7 hours. 1, 2
  • Must be separated from other oral medications by at least 3 hours. 2
  • Reserved for subacute or chronic hyperkalemia management. 2

• Avoid sodium polystyrene sulfonate (Kayexalate) due to delayed onset of action, limited efficacy, and risk of bowel necrosis and colonic ischemia. 2, 5, 6

Medication Management During Acute Episode

Medications to Hold Immediately (When K⁺ >6.5 mEq/L)

• Temporarily hold or reduce the following when serum potassium exceeds 6.5 mEq/L: 1, 2
  • RAAS inhibitors (ACE inhibitors, ARBs, mineralocorticoid receptor antagonists)
  • Non-steroidal anti-inflammatory drugs (NSAIDs)
  • Potassium-sparing diuretics (spironolactone, amiloride, triamterene)
  • Trimethoprim, heparin, beta-blockers
  • Potassium supplements and salt substitutes

Resumption and Optimization

• Restart RAAS inhibitors at a lower dose once potassium <5.0 mEq/L with concurrent potassium binder therapy. 1, 2
• Do not permanently discontinue RAAS inhibitors because of hyperkalemia; instead adjust dose and employ potassium binders. 1, 2
• For patients with cardiovascular disease or proteinuric chronic kidney disease, continue RAAS inhibitors while using potassium binders to control serum potassium. 1, 2

Chronic Hyperkalemia Management

Maintaining Life-Saving RAAS Inhibitors with Potassium Binders

• For patients on RAAS inhibitors with K⁺ 5.0–6.5 mEq/L, initiate patiromer or SZC and maintain RAAS inhibitor therapy unless an alternative treatable etiology is identified. 1, 2
• For patients on RAAS inhibitors with K⁺ >6.5 mEq/L, temporarily discontinue or reduce RAAS inhibitor; restart at a lower dose once K⁺ falls below 5.0 mEq/L with concurrent binder therapy. 1, 2
• Target maintenance potassium of 4.0–5.0 mEq/L to minimize mortality risk. 1, 2

Dietary Management

• Limit foods rich in bioavailable potassium, especially processed foods. 2
• Avoid salt substitutes containing potassium. 1, 2
• Avoid herbal supplements that raise K⁺ (alfalfa, dandelion, horsetail, nettle). 2
• Evidence linking dietary potassium intake to serum levels is limited; stringent dietary restrictions may not be necessary in patients receiving potassium binder therapy. 2

Monitoring Protocol

Acute Phase Monitoring

• Re-measure serum potassium 1–2 hours after insulin/glucose or beta-agonist therapy. 1, 2
• Continue potassium checks every 2–4 hours during the acute treatment period until levels stabilize. 1, 2
• Perform repeat ECGs if the initial presentation included cardiac abnormalities. 1, 2

Chronic Management Monitoring

• Check serum potassium 7–10 days after initiating or adjusting the dose of a RAAS inhibitor. 1, 2
• Check serum potassium within 1 week after starting or changing the dose of a potassium binder. 1, 2
• Tailor monitoring frequency to individual risk factors such as eGFR, heart failure status, diabetes control, and prior hyperkalemia episodes. 1, 2

Special Considerations

Diabetes-Specific Considerations

• Severe hyperglycemia (>1,000 mg/dL) creates a hyperosmolar extracellular environment that drives potassium out of cells, potentially producing extreme hyperkalemia (>7.0 mEq/L) even without marked acidosis. 1
• In diabetic patients, hyperkalemia risk is markedly increased due to impaired renal potassium excretion from diabetic nephropathy, hyporeninemic hypoaldosteronism (type IV RTA), and insulin-deficiency-mediated transcellular shifts. 1

Renal Failure Considerations

• Patients with chronic kidney disease, heart failure, and diabetes have substantially increased hyperkalemia risk. 2, 3, 6
• In advanced CKD (stage 4-5), patients tolerate higher potassium levels due to compensatory mechanisms, but maintaining target potassium 4.0–5.0 mEq/L minimizes mortality risk. 2

Critical Pitfalls to Avoid

• Do not delay calcium administration while awaiting repeat potassium values if ECG changes are present. 1, 2
• Never administer insulin without accompanying 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. 1, 2
• Do not permanently discontinue RAAS inhibitors; use potassium binders to maintain these life-saving medications. 1, 2
• Do not rely solely on ECG findings—they are highly variable and less sensitive than laboratory tests. 2