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. Troponin and creatine kinase-myocardial band (CK-MB) levels: These cardiac biomarkers are used to assess myocardial injury, such as in acute coronary syndrome. They are not appropriate for evaluating valvular abnormalities like mitral valve prolapse.

B. Computed tomography (CT) scan of the chest: A CT scan of the chest is used to evaluate pulmonary conditions, aortic dissection, or mediastinal structures, but it is not the test of choice for assessing cardiac valve function or structure.

C. 2D-echocardiography: Echocardiography is the primary diagnostic tool for evaluating mitral valve prolapse. It allows real-time visualization of valve structure and function, including leaflet motion and regurgitation severity, making it the most appropriate step after identifying a midsystolic click.

D. 12-lead electrocardiogram (ECG): An ECG can detect rhythm disturbances or signs of chamber enlargement but cannot diagnose structural valve issues. While useful as part of a general cardiac evaluation, it is not specific enough for diagnosing mitral valve prolapse.

• Congestive cardiomyopathy is the most likely condition given the client’s symptoms of labored breathing, bilateral leg edema, S3 gallop, and apical pulse displacement—all signs of fluid overload and decreased cardiac output associated with heart failure.
• Applying oxygen helps manage dyspnea and improves tissue oxygenation in clients with heart failure, especially when respiratory rate is elevated and breathing is labored.
• Requesting a chest x-ray allows for visualization of pulmonary congestion or cardiomegaly, both of which are common in heart failure and can guide further treatment decisions.
• Monitoring breath sounds helps detect improvement or worsening of pulmonary congestion, such as crackles or rales, which indicate fluid buildup in the lungs.
• Monitoring urine output evaluates kidney perfusion and fluid status, which reflects the effectiveness of heart failure treatment and overall cardiac output.
• Hypertrophic cardiomyopathy typically presents with exertional syncope or chest pain, not fluid overload signs like leg edema and S3 gallop. Apical displacement also favors dilation rather than hypertrophy.
• Dilated cardiomyopathy overlaps with congestive cardiomyopathy, but the broader term “congestive” aligns more clearly with fluid overload and heart failure signs.
• Restrictive cardiomyopathy involves impaired ventricular filling but does not usually present with displaced apical pulse or bilateral edema in early stages. It is also less common in this clinical setting.
• Starting IV fluids would worsen the client’s condition by increasing preload and exacerbating fluid overload in heart failure.
• Giving the client 80 mg of aspirin is more appropriate in acute coronary syndrome, not in managing cardiomyopathy or fluid retention.
• Preparing for cardioversion is indicated in arrhythmias like atrial fibrillation with hemodynamic instability, not in a hemodynamically stable patient with heart failure.
• Monitoring platelet count is not relevant to evaluating heart failure progression or response to treatment.
• Monitoring temperature is important for infection but does not reflect cardiac or fluid status in this context.
• Monitoring cerebral perfusion pressure is reserved for neurocritical care settings and is not appropriate for routine heart failure monitoring.