A client with acute kidney injury and a sharp decrease in urine output has a serum potassium of 6.0 mEq/L. Which order should the nurse administer intravenously right away to prevent cardiac arrest?

Principles of Emergency Management of Hyperkalemia

For a client with acute kidney injury whose serum potassium is 6.0 mEq/L, the priority intervention is dextrose solution mixed with insulin. This does not remove potassium from the body; rather, it is an emergency measure that rapidly shifts potassium into the cells to prevent life-threatening dysrhythmias and cardiac arrest.

In acute kidney injury, the glomerular filtration rate (GFR) falls abruptly and the kidneys' ability to excrete potassium is markedly reduced. When serum potassium exceeds 6.0 mEq/L, the resting membrane potential of cardiac muscle cells rises, electrical excitability of the heart becomes abnormal, and the risk of lethal dysrhythmias such as ventricular tachycardia, ventricular fibrillation, and asystole increases sharply ^[1].

Insulin activates the Na⁺-K⁺-ATPase pump located in the cell membrane. When this pump is activated, sodium (Na⁺) moves out of the cell and potassium (K⁺) moves into the cell. With intravenous insulin, cells throughout the body—including skeletal muscle—rapidly take up potassium from the bloodstream, temporarily lowering the serum potassium level within minutes. Dextrose is given along with the insulin to prevent the hypoglycemia that insulin can cause.

The supporting literature describes a client with severe hyperkalemia and a serum potassium as high as 8.7 mmol/L who reported only persistent nausea, with no EKG changes ^[1]. This illustrates an important clinical lesson: the clinical presentation of hyperkalemia does not always parallel the biochemical severity, and the absence of EKG changes is never reassuring. The laboratory value itself must therefore drive the decision to intervene emergently.

Why the Other Options Are Incorrect

A potassium-sparing diuretic (option 1), such as spironolactone, blocks sodium-potassium exchange in the distal tubule, decreasing potassium excretion and causing retention, so it is contraindicated in hyperkalemia. A vitamin D supplement (option 2) is used to manage secondary hyperparathyroidism in chronic kidney disease and has no direct effect on potassium levels. Total parenteral nutrition (TPN) (option 3) is given for nutritional support and may actually contain potassium depending on the formulation. A histamine receptor blocker (option 5) is used to suppress gastric acid secretion and is unrelated to the emergency management of hyperkalemia.