The vital signs for a client with heart failure (HF), who is admitted to the intensive care unit (ICU), are a temperature of 98.6° F (37°C), heart rate 125 beats/minute, respirations 22 breaths/minute, and blood pressure 140/50 mm Hg. The nurse determines the client's central venous pressure (CVP) and pulmonary artery wedge pressure (PAWP) are elevated. Which intervention should the nurse implement?
Initiate an IV bolus of 0.9% normal saline 500 mL.
Titrate IV dopamine at 8 mcg/kg/minute.
Administer furosemide 40 mg IV push (IVP).
Encourage a liberal PO fluid intake.
The Correct Answer is C
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.
Nursing Test Bank
Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is A
Explanation
A. Decreased cardiac output. Central venous pressure (CVP), also called right atrial pressure (RAP), reflects right ventricular preload and overall fluid status. An increasing CVP indicates fluid overload or impaired right ventricular function, both of which can lead to decreased cardiac output. Conditions such as right heart failure, pulmonary hypertension, or excessive fluid resuscitation can cause elevated CVP, reducing the heart’s ability to pump effectively and leading to poor systemic circulation.
B. Ineffective airway clearance. Airway clearance is not directly related to CVP measurements. While severe pulmonary conditions like ARDS or COPD can contribute to cardiac strain and right heart failure, the primary mechanism for rising CVP is cardiac dysfunction or fluid overload, not airway obstruction.
C. Ineffective peripheral tissue perfusion. Although decreased cardiac output can impair tissue perfusion, this choice is too broad. Increased CVP specifically reflects right-sided heart function and preload, making decreased cardiac output the more precise diagnosis related to the pathophysiologic mechanism.
D. Deficient fluid volume. A low CVP is associated with hypovolemia and fluid deficits, while an increasing CVP suggests fluid overload, heart failure, or venous congestion. Deficient fluid volume would cause a downward trend in CVP, not an increase.
Correct Answer is {"dropdown-group-1":"B","dropdown-group-2":"D"}
Explanation
- Compensated respiratory acidosis occurs when the lungs retain CO₂, causing acidosis, but the kidneys compensate by increasing bicarbonate (HCO₃⁻) levels. In this case, the pH is low, and the PaCO₂ is within normal limits, which does not indicate a respiratory issue or compensation. Compensation would require an elevated HCO₃⁻, which is not provided in the lab results.
- Compensated metabolic acidosis would require a low pH with a decreased PaCO₂, as the respiratory system compensates by increasing ventilation (hyperventilation) to "blow off" CO₂. Since the PaCO₂ in this case is within normal limits, no significant respiratory compensation has occurred yet, making this uncompensated metabolic acidosis instead.
- Uncompensated respiratory acidosis would present with a low pH and an elevated PaCO₂ (>45 mmHg) due to inadequate ventilation and CO₂ retention. Since the PaCO₂ here is 37 mmHg (within normal range), respiratory acidosis is unlikely. The metabolic component, rather than a respiratory problem, is driving the acidosis.
- Uncompensated metabolic acidosis is characterized by a low pH (7.23) and a normal PaCO₂ (37 mmHg), indicating a primary metabolic problem without sufficient respiratory compensation. In diabetic ketoacidosis (DKA), the lack of insulin results in fat breakdown and ketone production, leading to a drop in pH and metabolic acidosis. This client likely has DKA due to their history of type 1 diabetes and the lack of insulin administration.
- Kussmaul respirations are a compensatory response to metabolic acidosis, seen in conditions like DKA. However, they do not cause acidosis; instead, they are the body's attempt to correct it by exhaling CO₂. Since the ABG shows normal PaCO₂, there is no strong evidence of hyperventilation, suggesting compensation has not yet occurred.
- Starvation can lead to ketoacidosis due to prolonged fasting and fat metabolism, producing ketones. However, in type 1 diabetes, the primary issue is no insulin production, not caloric deprivation. The severity of metabolic acidosis in this client is more likely due to insulin deficiency rather than starvation.
- Tissue hypoxia leads to lactic acidosis, which results from anaerobic metabolism. This can be seen in conditions like sepsis or shock. However, in this case, the client has type 1 diabetes, and the more likely cause of acidosis is ketoacidosis due to insulin deficiency rather than hypoxia.
- A lack of insulin in type 1 diabetes prevents glucose uptake, forcing the body to break down fat, leading to ketone formation and metabolic acidosis. This matches the clinical scenario of a patient with a history of type 1 diabetes, hyperglycemia >500 mg/dL, and metabolic acidosis.
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