Hyperkalemia hub

Common scenarios

Workflow checklist

1. 1

   Confirm hyperkalemia and assess severity

   Document serum K (point-of-care or lab) and obtain a continuous ECG. Severity grading:

   • Mild (5.5–6.5 mEq/L): usually no ECG changes. Treat the underlying cause; drug bundle not always required.
   • Moderate (6.5–7.5 mEq/L): peaked T waves often present. Begin drug bundle if ECG changes are seen or rapid correction is not imminent.
   • Severe (> 7.5 mEq/L): prolonged PR, loss of P waves, wide QRS likely. Begin full drug bundle immediately.
   • Critical (any K with sine-wave QRS or severe bradyarrhythmia): peri-arrest. Calcium gluconate FIRST while preparing insulin/dextrose and fluids.
2. 2

   Calcium gluconate, membrane stabilization

   Onset 1–3 min, duration only 30–60 min. Does NOT lower K, raises the cardiac threshold potential to restore the gradient that hyperkalemia has narrowed. The "buy time" drug. ECG continuously throughout; STOP if bradycardia worsens.

   Use calcium GLUCONATE (10%), not chloride. Chloride is more potent and more cardiotoxic on a mL basis.

   Open calcium gluconate calculator →
3. 3

   Insulin + dextrose. K shifting

   Onset 15–30 min, duration 4–6 hr, typical K reduction 0.5–1.2 mEq/L. Insulin activates Na/K-ATPase, shifting K intracellularly. Concurrent dextrose prevents hypoglycemia. Followed by 2.5–5% dextrose CRI for 4–6 hr to prevent rebound.

   Regular crystalline insulin only. Monitor BG every 1 hr × 6 hr. Insulin shifts K but doesn't remove it, definitive treatment of the underlying cause is required.

   Open insulin/dextrose calculator →
4. 4

   Fluid therapy

   Aggressive volume resuscitation if hypovolemic (especially Addisonian crisis), then continued rehydration + maintenance. Fluid therapy:

   • Restores intravascular volume (the hypovolemia worsens the K problem)
   • Improves renal perfusion → restores urinary K excretion once obstruction is relieved
   • Dilutes serum K modestly
   • Corrects acidosis → reverses the extracellular K shift

   Fluid choice: 0.9% NaCl was traditionally recommended (no K, low concern about adding Ca to a calcium-containing line). Buffered isotonic crystalloids (LRS, Plasma-Lyte) contain small amounts of K (4–5 mEq/L) but are NOT contraindicated, the K load is trivial compared to the patient's existing K excess, and the buffered solutions correct acidosis faster, which itself helps lower K. Either is acceptable.

   Open fluid therapy calculator →
5. 5

   Definitive treatment of the underlying cause

   The drug bundle is bridging. The K problem resolves only when the underlying cause is corrected:

   • Feline UTO: decompressive cystocentesis (often done first, before or during drug bundle), then sedation + urethral catheter placement under sterile conditions, indwelling catheter for 24–48 hr.
   • Hypoadrenocorticism: dexamethasone 0.1–0.2 mg/kg IV (does NOT interfere with cortisol assay), aggressive fluid resuscitation with 0.9% NaCl, ACTH stimulation test for confirmation, then long-term mineralocorticoid replacement (DOCP injection or oral fludrocortisone).
   • AKI: address the inciting cause; consider mannitol or furosemide for fluid-refractory oliguria; dialysis if available for severe persistent AKI.
   • Tumor lysis syndrome: aggressive fluid therapy, allopurinol, urinary alkalinization (controversial in vet medicine).
6. 6

   Bicarbonate, rarely indicated

   Sodium bicarbonate is NOT a routine part of veterinary hyperkalemia management. The acidosis usually corrects with fluid therapy and obstruction relief. Bicarbonate use is associated with:

   • Worsened hypokalemia after K shifts back intracellularly
   • Hypocalcemia (alkalosis lowers ionized Ca)
   • Paradoxical CSF acidosis
   • Volume overload from the Na load

   Reserve for severe acidemia (pH < 7.0) unresponsive to fluid therapy and K reduction. If used: half-correction formula (NaHCO₃ mEq = 0.3 × kg × base deficit × 0.5), give slowly, recheck pH every 1–4 hours. Never co-infuse with calcium-containing fluids; precipitation as calcium carbonate.

7. 7

   Beta-2 agonists, adjunctive option

   Inhaled albuterol or terbutaline (IV/SQ) shifts K intracellularly via β₂-mediated Na/K-ATPase activation. Well-supported in human ICU literature; less commonly used in veterinary practice. Reasonable to consider as an adjunct when insulin/dextrose alone hasn't reduced K adequately and the underlying cause hasn't yet been corrected. Not first-line and not part of the standard veterinary hyperkalemia bundle.

8. 8

   Monitoring

   • Continuous ECG throughout active therapy
   • Serum K at 30 min and 1 hr after insulin, then every 2–4 hr until consistently < 5.5 mEq/L
   • Blood glucose every 1 hr × 6 hr after insulin bolus (rebound hypoglycemia window)
   • Blood pressure, mentation, perfusion parameters
   • Urine output (target > 1–2 mL/kg/hr once obstruction relieved or AKI improving)
   • Serum Na, glucose, BUN, creatinine, venous blood gas every 4–6 hr initially
   • Calcium and phosphorus once daily (post- obstruction diuresis can drop both)