Exhibits

Initial testing is complete, and the nurse is reviewing the results.

Choose the most likely options for the information missing from the statement by selecting from the lists of options provided.

The nurse determines that the client has

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as evidenced by ST depression on electrocardiogram and normal

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level.

A. Urinary output: Although decreased cardiac output can affect renal perfusion and lower urine output, it is not the immediate assessment after a sudden change in heart rate and pulse quality. Urine output trends over hours, not minutes, making it less useful for acute evaluation.

B. Pedal pulses: Pedal pulses assess peripheral circulation but are not as responsive to acute changes in central perfusion. Diminished pedal pulses may suggest poor perfusion, but the sudden rise in heart rate with weak radial pulse should prompt central hemodynamic assessment first.

C. Heart sounds: Heart sounds provide information about valve function and rhythm but may not detect subtle changes in perfusion status. While auscultation is important, it does not immediately quantify the impact of tachycardia and diminished pulse strength on blood pressure and perfusion.

D. Blood pressure: Assessing blood pressure is the most direct and immediate way to evaluate hemodynamic stability in the setting of sudden tachycardia with a weak pulse. Hypotension may indicate decreased cardiac output or early shock, requiring prompt recognition and intervention.

• Pulmonary embolism: The client’s recent orthopedic surgery, delayed mobility, obesity, and elevated D-dimer place her at high risk for PE. Her symptoms pleuritic chest pain, dyspnea, low oxygen saturation, anxiety, and sinus tachycardia are hallmark findings of PE.
• Elevate the head of the bed and administer oxygen by mask or nasal cannula: Supporting oxygenation is the immediate priority in a suspected PE. Elevating the head of the bed improves ventilation, while oxygen therapy helps correct hypoxemia until more definitive treatment begins.
• Prepare to initiate anticoagulation therapy: Anticoagulation is the frontline treatment for pulmonary embolism to prevent clot progression and recurrence. It is initiated as soon as PE is suspected, even before imaging confirms the diagnosis.
• Arterial blood gas: ABG will help assess the extent of oxygenation impairment and respiratory compromise caused by the embolism. Hypoxemia and respiratory alkalosis are commonly seen in acute PE.
• Pain score monitoring allows evaluation of symptom progression and the effectiveness of supportive measures. Pain may persist or worsen with increased clot burden, making regular assessment necessary.
• Myocardial infarction: While chest pain and tachycardia can suggest MI, the troponin levels are normal, the ECG only shows sinus tachycardia (no ST changes), and the pain is pleuritic and positional atypical of MI. The elevated D-dimer and recent surgery point more strongly toward PE.
• Anxiety: Although the client is anxious and dyspneic, these are more likely symptoms of the underlying cardiopulmonary issue rather than the primary diagnosis. Anxiety alone would not cause hypoxia, crackles, and elevated D-dimer.
• Sepsis: Sepsis might present with hypotension and elevated WBC, but this client’s vitals and CBC are within range. There is no evidence of infection, fever, or systemic inflammatory response that would indicate sepsis over PE.
• Instruct client to bear down to decrease heart rate: This vagal maneuver (Valsalva) is appropriate for supraventricular tachycardia, not for sinus tachycardia due to hypoxia. It could worsen symptoms in a client with compromised oxygenation like PE.
• Prepare client for drawing blood cultures: Blood cultures are relevant when infection or sepsis is suspected. The client shows no signs of infection (e.g., fever, chills, elevated WBC), so this action does not address the most likely diagnosis.
• Place client in Trendelenburg position: Positioning such as Trendelenburg is not appropriate for PE and can worsen respiratory function. Instead, upright positioning helps improve lung expansion and oxygenation.
• Skin: Skin color and temperature can indicate perfusion but are nonspecific. They won't directly measure improvement or deterioration in a client with PE, especially once oxygen therapy is initiated.
• Clotting factors: While clotting studies are monitored when administering anticoagulants, they are not immediate indicators of PE progression or treatment response. They are important later but not primary for initial monitoring.
• Cardiac enzymes: These are essential in diagnosing myocardial infarction, not PE. Since troponin is within normal limits, monitoring enzymes will not provide relevant information in this context.