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Symptomatic or ECG-significant hyperkalemia is life-threatening. The FIRST step is myocardial stabilization with IV calcium (e.g., calcium gluconate 1–2 g), which counteracts membrane excitability within minutes but does not lower serum potassium. Immediately follow with intracellular shifting strategies—regular insulin (e.g., 10 units IV) plus dextrose to prevent hypoglycemia; consider nebulized albuterol and/or sodium bicarbonate if acidosis. Begin or continue aggressive isotonic IV fluids to promote renal excretion and avoid potassium-containing solutions. Arrange definitive potassium removal with loop diuretics if euvolemic and responsive kidneys, potassium binders as adjuncts, and early nephrology consult for dialysis if refractory or in renal failure. Sodium polystyrene alone (Option A) has delayed onset and questionable efficacy for emergencies. Allopurinol (Option C) treats uric acid formation, not acute hyperkalemia. Stopping fluids (Option D) worsens renal clearance and TLS risk. APRNs must implement a TLS pathway: frequent labs, cardiac monitoring, rasburicase for hyperuricemia when appropriate, and clear thresholds for dialysis.