A patient is scheduled for an electromyography (EMG) test. The nurse is preparing the patient for the procedure. Which of the following actions should the nurse take to ensure the patient's safety and comfort during the EMG?

A. The nurse anticipates tachycardia due to the metabolic disturbances and physiological stress associated with acute renal failure. Elevated potassium levels (6.8 mEq/L) can irritate the myocardium, leading to compensatory heart rate increases or dysrhythmias. Additionally, the initial hypovolemia from the motorcycle accident triggers sympathetic nervous system activation, maintaining a high heart rate.

B. While renal disease can eventually lead to fluid retention, hypertension is not necessarily anticipated in the acute phase following severe hypovolemic shock. The client’s history of massive hemorrhage and hypovolemia from the accident suggests a risk for persistent hypotension or labile blood pressure.

C. Confusion is a frequent assessment finding in clients with advancing renal impairment and elevated nitrogenous wastes. The accumulation of urea (BUN 25 mg/dL) and other toxins crosses the blood-brain barrier, resulting in uremic encephalopathy. Metabolic acidosis, which often accompanies a low GFR of 51 mL/min/1.73 m2, further depresses the central nervous system.

D. Decreased urinary output is the hallmark clinical sign of AKI, reflecting a significant drop in renal perfusion and filtration capacity. With a GFR reduced to 51 mL/min/1.73 m2 and elevated creatinine of 2.0 mg/dL, the kidneys are unable to effectively excrete fluid. The client is likely in the oliguric phase, where the volume of urine produced is insufficient to maintain homeostasis.

E. There is no evidence in the record to suggest oxygen requirements would be decreasing; in fact, they may increase. The presence of an elevated WBC (11,500 mm3) and the stress of a spinal cord injury (T8 severance) increase metabolic demands. Furthermore, fluid overload from AKI can lead to pulmonary edema, which would worsen rather than improve oxygenation status.

A. Continue heparin therapy and monitor platelet counts: Heparin-induced thrombocytopenia (HIT) is an immune-mediated adverse reaction in which antibodies form against the heparin–platelet factor 4 complex, leading to platelet activation and thrombosis. Continuing heparin can worsen platelet consumption and increase the risk of life-threatening thromboembolic events.

B. Discontinue heparin immediately and start an alternative anticoagulant: The priority intervention in suspected HIT is the immediate cessation of all heparin products to prevent further antibody-mediated platelet activation. Because HIT creates a prothrombotic state, an alternative non-heparin anticoagulant is initiated to reduce the risk of DVT or PE.

C. Administer platelet transfusion to manage thrombocytopenia: In HIT, thrombocytopenia results from platelet activation and consumption, not from decreased production. Transfusing platelets may exacerbate thrombosis by providing additional substrate for clot formation. Platelet transfusions are generally avoided unless there is significant active bleeding.

D. Administer intravenous fluids to prevent dehydration: While maintaining adequate hydration is important for overall circulatory stability, IV fluids do not address the immune-mediated platelet activation or thrombotic risk associated with HIT. The immediate threat is thrombosis, which requires stopping heparin and initiating alternative anticoagulation.