A client is admitted to the critical care unit (CCU) with a third degree complete heart block. A temporary transvenous pacemaker is inserted by the healthcare provider (HCP). An hour after pacemaker insertion, the device stops sensing the client's intrinsic heart rate. Which action should the nurse implement first?

A. Initiate an IV bolus of 0.9% normal saline 500 mL. The client already has elevated CVP and PAWP, which indicate fluid overload and poor cardiac function. Giving a fluid bolus would worsen pulmonary congestion, edema, and respiratory distress. Fluid restriction, rather than additional IV fluids, is usually necessary in decompensated heart failure.
B. Titrate IV dopamine at 8 mcg/kg/minute. Dopamine is a vasopressor and inotropic agent that increases blood pressure and cardiac output. However, the client has an elevated blood pressure (140/50 mm Hg) and signs of fluid overload, making dopamine unnecessary. Increasing contractility could further stress the failing heart and worsen congestion.
C. Administer furosemide 40 mg IV push (IVP). Furosemide (a loop diuretic) is the best intervention for fluid overload in heart failure. Elevated CVP and PAWP suggest pulmonary congestion and excess intravascular volume, which furosemide helps relieve by reducing preload and promoting diuresis. This intervention improves breathing, reduces blood pressure, and decreases cardiac workload.
D. Encourage a liberal PO fluid intake. Clients with heart failure often require fluid restriction to prevent worsening edema and pulmonary congestion. Encouraging excessive oral fluid intake would worsen fluid overload and should be avoided.

A. White blood cell differential. Although infection is a common precipitating factor for DKA, an elevated WBC count is common in DKA due to stress, dehydration, and inflammation rather than infection itself. While a WBC differential may be done if infection is suspected, it is not a primary test for DKA management.
B. Hemoglobin A1C. Hemoglobin A1C (HbA1c) reflects long-term glucose control (past 2-3 months) but does not provide immediate information about the current metabolic status or severity of DKA. While it may be useful in assessing overall diabetes management, it is not essential for acute DKA treatment.
C. Serum electrolytes. Patients with DKA experience significant electrolyte imbalances, particularly potassium depletion due to osmotic diuresis and insulin deficiency. Monitoring serum sodium, potassium, and bicarbonate is crucial for guiding fluid and electrolyte replacement therapy. Potassium levels may appear normal or high initially due to acidosis but typically drop with insulin administration.
D. Urine culture. A urine culture is only indicated if a urinary tract infection (UTI) is suspected as a trigger for DKA. However, routine urine culture is not required in every case of DKA unless there are symptoms of infection such as fever, dysuria, or pyuria.
E. Anion gap. DKA is a form of high anion gap metabolic acidosis, caused by the accumulation of ketones. The anion gap (AG) is calculated as (Na⁺ - [Cl⁻ + HCO₃⁻]), with a value >12 mEq/L indicating metabolic acidosis. Monitoring the anion gap helps assess the severity of acidosis and guide treatment progress, as a decreasing anion gap suggests resolution of ketosis.
F. Urine ketones. Urine ketone testing helps confirm the presence of ketoacidosis, particularly in the initial stages of DKA diagnosis. While serum beta-hydroxybutyrate is a more accurate indicator of ketone levels, urine ketones remain useful for initial screening and monitoring treatment response as they decrease with appropriate management.