Hyperkalemia: Stabilize, Shift, Remove

Dangerous potassium is a rhythm problem first. Treat in three moves—stabilize the myocardium,shift potassium intracellularly, and remove potassium from the body—while you fix the cause and prevent rebound.

Confirm It’s Real (Pseudohyperkalemia is common)

• Repeat a plasma/serum K⁺ promptly if hemolysis suspected (difficult draw, prolonged tourniquet, fist clenching).
• Look for thrombocytosis/leukocytosis causing spuriously high K⁺ in serum—use plasma sample if needed.

Read the ECG (but don’t wait if unstable)

• Typical progression: peaked T waves → PR prolongation → QRS widening → sine-wave → VF/asystole. Sequence can be atypical—treat the patient.
• Immediate calcium for ECG changes or severe hyperkalemia even before the repeat lab returns.

STABILIZE — IV Calcium

• Calcium gluconate 1 g IV over 5–10 min (may repeat in 5–10 min if ECG not improved).
• Calcium chloride 1 g IV (via central line preferred) for arrest or profound instability.
• Effect begins within minutes and lasts ~30–60 min—gives you time to shift/remove K⁺.
• Traditional caution in digoxin toxicity; many centers give calcium if life-threatening arrhythmia—consult tox if uncertain.

SHIFT — Drive K⁺ into Cells

• Insulin + dextrose: Regular insulin 10 units IV + dextrose 25 g (e.g., 50 mL D50) if BG <250 mg/dL; add D10 infusion if hypoglycemia risk. Onset 15–30 min, lasts 2–6 h.
• Nebulized albuterol (beta-agonist): 10–20 mg via neb over 10–15 min (avoid in significant tachyarrhythmia). Onset ~30 min.
• Sodium bicarbonate IV if metabolic acidosis (e.g., DKA, uremic acidosis); limited effect without acidosis.

REMOVE — Get K⁺ out of the Body

• Loop diuretics (e.g., furosemide) if euvolemic/overloaded and kidneys can respond; give with fluids as appropriate.
• Potassium binders (use local formulary):
  • Patiromer PO (hours to effect; good for non-emergent control/prevention).
  • Sodium zirconium cyclosilicate PO (can start lowering K⁺ within 1–2 h; watch Na⁺ load/edema).
• Hemodialysis: definitive for severe/refractory hyperkalemia, especially with kidney failure, massive tissue breakdown, or when medical therapy fails.

Who Needs Immediate Aggressive Therapy?

• K⁺ ≥6.5 mmol/L or any ECG changes (peaked T, QRS widening, brady, sine-wave).
• Rapid rise in K⁺ (tumor lysis, rhabdomyolysis), severe AKI/CKD, or symptomatic weakness/paresthesias.

Monitoring & Rebound Prevention

• Cardiac monitor. Recheck K⁺ every 1–2 hours initially; watch glucose every 30–60 min after insulin.
• Anticipate rebound as shifts wear off—ensure a removal strategy (binder/diuresis/dialysis) is in place.
• Correct co-factors: hypocalcemia, metabolic acidosis, and hyperglycemia.

Why Did K⁺ Rise? (Fix the cause)

• Decreased excretion: AKI/CKD, hypoaldosteronism (ACEi/ARB, heparin, adrenal disease), K⁺-sparing diuretics (spironolactone, eplerenone, amiloride), trimethoprim, NSAIDs.
• Shift out of cells: DKA, severe acidosis, beta-blockers, succinylcholine, digoxin toxicity.
• Excess load: supplements, salt substitutes, blood products, tumor lysis, rhabdomyolysis.

Disposition

• Admit/ICU for ECG changes, K⁺ ≥6.5, ongoing tissue breakdown, renal failure, or need for dialysis.
• Discharge only after normalization, identified cause addressed (med changes), stable ECG, reliable follow-up, and low rebound risk.

Patient FAQs

“Why do I need calcium if my calcium is normal?” It stabilizes the heart’s electrical system against potassium’s effects—it doesn’t treat blood calcium.

“Will this come back?” It can if we only shift K⁺; that’s why we also remove K⁺ and fix the cause (kidneys, meds, acidosis).

References & Notes

Common ED/ward sequence: calcium for membrane stabilization, insulin/dextrose ± beta-agonist ± bicarbonate to shift, plus diuretics/binders/dialysis to remove. Monitor closely for rebound and hypoglycemia. Local protocols vary—follow institutional guidance. Educational only.