A nurse is caring for a 65-year-old patient with acute kidney injury (AKI) in the oliguric phase, experiencing urine output of 200 mL in the past 24 hours. Laboratory results show: BUN 85 mg/dL, creatinine 4.2 mg/dL, potassium 6.8 mEq/L, and phosphorus 7.5 mg/dL. The patient appears restless and reports muscle weakness. Which nursing intervention should be the highest priority?

In a patient with oliguric AKI, a serum potassium level of 6.8 mEq/L is a critical emergency. The primary nursing responsibility is to recognize that neuromuscular symptoms like restlessness and muscle weakness are prodromal signs of cardiac toxicity. The priority is to protect the myocardium from lethal arrhythmias.

1. Continuous Cardiac Monitoring: Immediately place the patient on a cardiac monitor. Assess the rhythm strip for signs of hyperkalemia, including peaked T-waves, widened QRS complexes, and loss of P-waves. These changes can rapidly deteriorate into a sine-wave pattern, ventricular tachycardia, or asystole.
2. Prepare for Emergency Interventions: Anticipate and prepare for the administration of intravenous calcium gluconate or calcium chloride. This does not lower the potassium level but directly antagonizes the cardiotoxic effects, stabilizing the cardiac membrane. Ensure IV access is patent.
3. Shift Potassium Intracellularly: Following cardiac stabilization, prepare to administer IV regular insulin with dextrose (to prevent hypoglycemia) and inhaled beta-2 agonists (e.g., albuterol) as prescribed to temporarily shift potassium back into the cells.
4. Facilitate Potassium Elimination: Prepare for definitive treatments to remove potassium from the body, such as administering oral or rectal sodium polystyrene sulfonate (a cation exchange resin), loop diuretics if the patient has residual renal function, or emergent hemodialysis.

• Fluid Administration: Do not encourage or administer large volumes of fluid. The patient is in the oliguric phase and cannot excrete the fluid, which can rapidly lead to pulmonary edema, hypertension, and heart failure.
• Non-Emergent Medications: While phosphate binders and dietary protein restriction are important components of the AKI treatment plan, they are secondary interventions. They do not address the immediate, life-threatening risk of a potassium level of 6.8 mEq/L and should be implemented after the patient is stabilized.

Closely monitor vital signs, hourly urine output, and serial electrolyte panels. Assess for signs of fluid overload, such as crackles on auscultation, dyspnea, and dependent edema. Maintain strict intake and output records. Ensure the patient's call light is within reach and provide reassurance, as anxiety can worsen the physiological stress response.