A client with heart failure reports dyspnea and anxiety. Upon examination the client is tachycardic and has crackles throughout bilateral lung fields. Which actions will the nurse take now? Select all that apply.
Monitor urine output
Assess pulse oximetry
Check PT/INR
Infuse 0.9% NS with 20 mEq KCl at 50 ml/hr
Administer 40 mg furosemide IV now
Correct Answer : A,B,E
a. Monitor urine output: Monitoring urine output is important in clients with heart failure to assess renal perfusion and renal function. Decreased urine output may indicate worsening heart failure or inadequate response to treatment. Therefore, monitoring urine output is appropriate in this situation to assess the client's fluid status and response to therapy.
b. Assess pulse oximetry: Assessing pulse oximetry is essential to evaluate the client's oxygen saturation levels, especially in a client presenting with dyspnea and crackles throughout bilateral lung fields. Decreased oxygen saturation may indicate respiratory compromise or worsening heart failure. Therefore, assessing pulse oximetry is necessary to monitor the client's respiratory status and guide interventions.
c. Check PT/INR: Checking PT/INR (Prothrombin Time/International Normalized Ratio) is not indicated in this situation. PT/INR monitoring is typically performed in clients on anticoagulant therapy such as warfarin to assess coagulation status and therapeutic levels. It is not directly relevant to the client's current presentation of dyspnea, tachycardia, and crackles.
d. Infuse 0.9% NS with 20 mEq KCl at 50 ml/hr: Infusing normal saline (0.9% NS) with potassium chloride (KCl) is not appropriate based solely on the client's presentation of dyspnea, anxiety, tachycardia, and crackles. While fluid and electrolyte balance are important considerations in heart failure management, administering IV fluids and electrolytes should be guided by the client's fluid status, electrolyte levels, and response to treatment.
e. Administer 40 mg furosemide IV now: Administering furosemide IV (intravenous loop diuretic) is appropriate in this situation to manage the client's symptoms of dyspnea and crackles indicative of fluid overload in heart failure. Furosemide helps promote diuresis and reduce fluid volume, thereby alleviating symptoms of congestion and improving respiratory distress.
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Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is ["A","B","C","E"]
Explanation
a. Abdominal distension: Abdominal distension can occur in cases of severe digoxin toxicity due to its effects on gastrointestinal motility. Digoxin toxicity can lead to nausea, vomiting, and abdominal discomfort, which can contribute to abdominal distension. Therefore, abdominal distension is consistent with digoxin toxicity.
b. Digoxin level 4.1 ng/ml (0.8-2.0ng/ml): Digoxin levels above the therapeutic range (0.8-2.0 ng/ml) indicate digoxin toxicity. A level of 4.1 ng/ml is significantly higher than the therapeutic range, confirming digoxin toxicity.
c. Blurry vision: Blurry vision is a common symptom of digoxin toxicity. Visual disturbances, such as yellow or green halos around lights or changes in color vision, can occur due to digoxin's effects on the optic nerve. Therefore, blurry vision is consistent with digoxin toxicity.
d. Increased platelet level: Digoxin toxicity typically does not cause an increase in platelet levels. Instead, it can lead to thrombocytopenia (a decrease in platelet levels) due to its effects on bone marrow function. Therefore, increased platelet levels are not consistent with digoxin toxicity.
e. Arrhythmia: Digoxin toxicity can cause various cardiac arrhythmias, including atrial tachycardia, atrioventricular block, and ventricular tachycardia. Therefore, experiencing arrhythmias is consistent with digoxin toxicity.
Correct Answer is D
Explanation
Decreasing level of consciousness: This assessment finding is consistent with respiratory acidosis, especially if it is severe. In respiratory acidosis, carbon dioxide (CO2) levels in the blood increase, leading to respiratory depression and potential alterations in consciousness due to hypercapnia. Therefore, a decreasing level of consciousness is a possible finding in a client with respiratory acidosis.
b. Bradycardia: Bradycardia is not typically associated with respiratory acidosis. In fact, it is more commonly associated with respiratory alkalosis, where hyperventilation can lead to decreased CO2 levels and subsequent compensatory metabolic alkalosis.
c. Fever: Fever is not a direct consequence of respiratory acidosis. It may occur in response to an underlying infection or inflammation, which could exacerbate respiratory symptoms in a client with COPD. However, it is not a specific finding associated with respiratory acidosis itself.
d. ABG: pH 7.31, PaCO2 42 mmHg, HCO3 19 mEq/L: This ABG result confirms respiratory acidosis. The pH is below the normal range (acidosis), the PaCO2 is elevated (indicating respiratory acidosis), and the HCO3 is decreased (indicating compensation through renal mechanisms). This ABG finding supports the diagnosis of respiratory acidosis in a client with COPD.
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