A 58-year-old man is admitted to the unit with a 3-day history of decreased urine output and generalized edema. He was diagnosed with type 2 diabetes mellitus 10 years ago and takes metformin. He also reports recently taking an over-the-counter cold remedy. His findings are shown below. Which intervention should the nurse implement first?

This client has hyperkalemia (6.4 mEq/L) secondary to acute kidney injury and is at high risk for cardiac dysrhythmias. Following the ABC priority framework, the nurse must first apply cardiac (ECG) monitoring to detect life-threatening dysrhythmias. ECG changes associated with hyperkalemia (peaked T waves, widened QRS) signal an emergency requiring immediate intervention.

Core concept: Emergency management of acute kidney injury with hyperkalemia

This client has classic risk factors for acute kidney injury (AKI): a 10-year history of diabetes and recent use of a cold remedy (likely containing a nonsteroidal anti-inflammatory drug, or NSAID). Laboratory results showing BUN 62 mg/dL and creatinine 4.8 mg/dL indicate severely impaired renal function, and potassium 6.4 mEq/L represents severe hyperkalemia requiring immediate intervention.

Hyperkalemia is most dangerous because it directly affects the heart's electrical conduction system and can precipitate life-threatening dysrhythmias. As serum potassium rises, the resting membrane potential of myocardial cells becomes less negative (partial depolarization), initially increasing myocardial excitability; over time, however, sodium channels become inactivated, conduction slows, and cardiac arrest may follow. Therefore, when serum potassium exceeds 6.0 mEq/L or ECG changes appear, protecting the heart takes priority over every other intervention.

Option 4, applying cardiac monitoring, is the first action because it is the only way to identify in real time whether cardiotoxicity is present and how far it has progressed. On the ECG, hyperkalemia progresses from peaked T waves (T-peaking) to loss of P waves, widening of the QRS complex, and finally a sine wave pattern that heralds imminent cardiac arrest. Resuscitation guidelines likewise treat cardiac arrest from acute hyperkalemia as a special circumstance requiring modification of the standard algorithm, emphasizing rapid recognition and treatment. Without ECG monitoring, the onset of these lethal changes can be missed.

Using the concept of BRASH syndrome (Bradycardia, Renal failure, AV nodal blockade, Shock, Hyperkalemia): when hyperkalemia develops in the setting of renal failure, AV nodal blocking effects are amplified, creating a vicious cycle of bradycardia and shock. This client is not yet bradycardic (pulse 98 beats/min), but with a blood pressure of 168/94 mmHg and rapidly declining renal function, monitoring the effect of hyperkalemia on cardiac conduction is the most urgent priority.

The remaining options are not appropriate for the following reasons. Verifying a diuretic order (option 1) and starting a 24-hour urine collection (option 2) are important for determining the cause of the kidney injury and guiding treatment, but neither should precede addressing the immediately life-threatening cardiotoxicity of hyperkalemia. Teaching a potassium-restricted diet (option 3) is a long-term management strategy and is ineffective in the acute phase when potassium has already risen to 6.4 mEq/L. An IV infusion of 0.9% normal saline (option 5) is used primarily for prerenal AKI accompanied by hypovolemia; this client has hypertension and generalized edema indicating fluid volume overload, so fluid administration risks worsening pulmonary edema.

Emergency management of hyperkalemia proceeds in three steps: stabilize the myocardium, shift potassium into the cells, and remove potassium from the body. Once cardiac monitoring reveals signs of cardiotoxicity such as peaked T waves or a widened QRS, calcium gluconate should be given IV immediately to stabilize the myocardial cell membrane. This does not lower the potassium level; rather, it temporarily raises the cardiac threshold against elevated potassium and prevents dysrhythmias. Insulin with dextrose and beta-2 agonists are then given to shift potassium intracellularly, and dialysis ultimately removes the excess potassium from the body [2, 3].