Management of Acute Hyperkalemia

For acute hyperkalemia, immediately stabilize the cardiac membrane with IV calcium, shift potassium intracellularly with insulin-glucose and nebulized albuterol, then remove potassium from the body using loop diuretics (if adequate renal function), potassium binders, or emergent hemodialysis—with treatment intensity determined by serum potassium level, ECG changes, and clinical context.

Step 1: Assess Severity and Determine Treatment Urgency

Classification by Serum Potassium

Mild hyperkalemia: 5.0–5.9 mEq/L 1
Moderate hyperkalemia: 6.0–6.4 mEq/L 1
Severe hyperkalemia: ≥6.5 mEq/L 1, 2

ECG Changes Override Laboratory Values

Peaked T waves, flattened P waves, prolonged PR interval, or widened QRS complex mandate immediate treatment regardless of the absolute potassium level 1, 2. ECG abnormalities indicate urgent cardiac risk even when potassium is only moderately elevated 1.
Absent or atypical ECG changes do not exclude the need for immediate intervention 3. The rate of potassium rise and the patient's underlying cardiac disease are as important as the absolute value 1.

High-Risk Populations Requiring Aggressive Management

Chronic kidney disease, heart failure, diabetes, or history of hyperkalemia 1
Patients on RAAS inhibitors, NSAIDs, potassium-sparing diuretics, or beta-blockers 1
Atrioventricular heart block or other cardiac conduction abnormalities 1

Step 2: Cardiac Membrane Stabilization (Immediate—Within 1–3 Minutes)

Intravenous Calcium Gluconate

Administer calcium gluconate 10% (15–30 mL) IV over 2–5 minutes for any patient with ECG changes or serum potassium ≥6.5 mEq/L 1, 2.
Onset of action: 1–3 minutes; duration: 30–60 minutes 1, 2.
Calcium does NOT lower serum potassium—it only temporarily stabilizes the cardiac membrane 1, 2.
If no ECG improvement within 5–10 minutes, repeat the dose 1, 2.

Alternative: Calcium Chloride

Calcium chloride 10% (5–10 mL, 500–1000 mg) IV over 2–5 minutes is preferred when central venous access is available because it provides a more rapid increase in ionized calcium than calcium gluconate 2.
Pediatric dosing: Calcium chloride 20 mg/kg (0.2 mL/kg of 10% solution) IV with continuous ECG monitoring 1, 2.

Critical Safety Considerations

Do NOT mix calcium with sodium bicarbonate in the same IV line—precipitation will occur 1, 2.
Use calcium cautiously in patients with elevated serum phosphate (e.g., tumor lysis syndrome) due to risk of calcium-phosphate precipitation in tissues 1, 2.
Monitor heart rate during calcium administration and stop if symptomatic bradycardia develops 2.

Step 3: Shift Potassium Intracellularly (Onset 15–60 Minutes)

Insulin with Dextrose (First-Line Intracellular Shift Agent)

Administer 10 units regular insulin IV push with 25 g dextrose (50 mL D50W) 1, 2, 3.
Onset: 15–30 minutes; peak effect: 30–60 minutes; duration: 4–6 hours 1, 2.
Expected potassium reduction: 0.5–1.2 mEq/L 1.
Glucose must always accompany insulin to prevent life-threatening hypoglycemia 1, 2.
Monitor blood glucose closely after administration, especially in patients with low baseline glucose, no diabetes, female sex, or impaired renal function 1, 2.

Nebulized Albuterol (Adjunctive Intracellular Shift Agent)

Administer albuterol 10–20 mg nebulized in 4 mL over 10–15 minutes 1, 2, 3.
Onset: ~30 minutes; duration: 2–4 hours 1, 2.
Expected potassium reduction: 0.5–1.0 mEq/L 1, 2.
The combination of insulin-glucose plus nebulized albuterol produces a greater potassium reduction than either agent alone 1, 2.
Albuterol can be repeated every 2 hours if needed 1, 2.
Most common side effect: sinus tachycardia 2.

Sodium Bicarbonate (ONLY with Concurrent Metabolic Acidosis)

Administer sodium bicarbonate 50 mEq IV over 5 minutes ONLY when arterial pH <7.35 and serum bicarbonate <22 mEq/L 1, 2, 3.
Onset: 30–60 minutes 1, 2.
Sodium bicarbonate is ineffective as monotherapy for hyperkalemia without metabolic acidosis 1, 2, 3.
Do NOT use sodium bicarbonate in patients without documented acidosis—it wastes time and provides no benefit 1, 2.

Step 4: Remove Potassium from the Body (Definitive Treatment)

Loop Diuretics (Renal Excretion—Effective Only with Adequate Kidney Function)

Administer furosemide 40–80 mg IV to increase renal potassium excretion in patients with eGFR >30 mL/min and adequate urine output 1, 2.
Loop diuretics should be titrated to maintain euvolemia, not primarily for potassium management 1.
Thiazide diuretics can also promote urinary potassium excretion 1.

Potassium Binders (Gastrointestinal Excretion)

Sodium Zirconium Cyclosilicate (SZC/Lokelma)—Preferred for Urgent Scenarios

Initial dosing: 10 g three times daily for 48 hours, then 5–15 g once daily for maintenance 1.
Onset of action: ~1 hour 1.
SZC reduces serum potassium within 1 hour of a single 10-g dose and is effective for both acute (≥5.8 mEq/L) and chronic hyperkalemia 1.
SZC may improve metabolic acidosis by increasing ammonium excretion from the intestinal tract 1.

Patiromer (Veltassa)—Preferred for Sub-Acute/Chronic Management

Initial dosing: 8.4 g once daily with food, titrated up to 25.2 g daily based on potassium levels 1.
Onset of action: ~7 hours 1.
Patiromer must be separated from other oral medications by at least 3 hours to avoid reduced absorption 1.
Patiromer causes hypomagnesemia and hypercalcemia—monitor magnesium levels closely 1.

Sodium Polystyrene Sulfonate (Kayexalate)—AVOID

Sodium polystyrene sulfonate is associated with intestinal ischemia, colonic necrosis, and a doubling of risk for serious gastrointestinal adverse events 1, 4, 5.
Sodium polystyrene sulfonate has limited efficacy data and should be avoided in favor of newer potassium binders 1, 4, 5.

Emergent Hemodialysis (Most Effective Method for Severe Hyperkalemia)

Absolute Indications for Hemodialysis

Serum potassium >6.5 mEq/L unresponsive to medical therapy 1, 2
Oliguria or anuria 1, 2
End-stage renal disease 1, 2
Ongoing potassium release (e.g., tumor lysis syndrome, rhabdomyolysis) 1, 2
Severe renal impairment (eGFR <15 mL/min) 1, 2
Persistent ECG changes despite medical management 1, 2

Hemodialysis vs. Continuous Renal Replacement Therapy (CRRT)

Hemodialysis is the most reliable and effective method for potassium removal 1, 2, 5.
In hemodynamically unstable patients (e.g., hypotensive, requiring vasopressor support), CRRT is preferred over intermittent hemodialysis because it minimizes rapid fluid shifts and reduces the risk of intradialytic hypotension 1, 2.

Step 5: Medication Management During Acute Episode

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

RAAS inhibitors (ACE inhibitors, ARBs, mineralocorticoid receptor antagonists) 1, 2
NSAIDs 1, 2
Potassium-sparing diuretics (spironolactone, amiloride, triamterene) 1, 2
Trimethoprim-containing agents 1, 2
Heparin 1, 2
Beta-blockers 1, 2
Potassium supplements and salt substitutes 1, 2

Resumption and Optimization After Acute Resolution

Restart RAAS inhibitors at a lower dose once potassium <5.0 mEq/L 1, 2.
Initiate a potassium binder (SZC or patiromer) to enable continuation of life-saving RAAS therapy 1, 2.
RAAS inhibitors provide mortality benefit in cardiovascular and renal disease and should NOT be permanently discontinued 1, 2.

Step 6: Monitoring Protocol

Acute Phase

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

Post-Acute Phase

Check potassium within 1 week after initiating or escalating RAAS inhibitors 1.
Reassess 7–10 days after starting a potassium binder 1.
Tailor monitoring frequency to renal function, heart failure status, diabetes, or prior hyperkalemia episodes 1.

Critical Pitfalls to Avoid

Do NOT delay calcium administration while awaiting repeat potassium levels when ECG changes are present 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 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 1.

What is the step‑by‑step management of acute hyperkalemia, including indications for intravenous calcium gluconate, insulin with dextrose, nebulised albuterol, sodium bicarbonate, loop diuretics, potassium binders, and emergent haemodialysis?

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