A 51-year-old male client with pneumonia has undergone several days of antibiotic and respiratory treatment. Given the following assessment findings, mark whether they indicate that the treatment was effective or ineffective:
PaCO2 55 mm Hg on a blood gas
Rhonchi in the right lung
Oxygen saturation greater than 94%
Client ambulates without shortness of breath
Correct Answer : C,D
Choice A rationale:
PaCO2 55 mm Hg on a blood gas indicates ineffective treatment. Normal PaCO2 levels range from 35-45 mm Hg.
Elevated PaCO2 (hypercapnia) suggests that the lungs are not effectively removing carbon dioxide from the body. This can be due to various factors, including:
Incomplete resolution of pneumonia Airway obstruction
Impaired respiratory muscle function
Choice B rationale:
Rhonchi in the right lung indicates ineffective treatment.
Rhonchi are coarse, rattling sounds heard in the lungs during auscultation.
They are often associated with mucus accumulation in the airways, which can occur in pneumonia.
The presence of rhonchi suggests that inflammation and mucus production persist, despite antibiotic and respiratory therapy.
Choice C rationale:
Oxygen saturation greater than 94% indicates effective treatment. Normal oxygen saturation levels are typically 95% or higher.
A saturation of 94% or above suggests that the lungs are able to effectively oxygenate the blood. This is a positive sign that the pneumonia is responding to treatment.
Choice D rationale:
Client ambulates without shortness of breath indicates effective treatment. Shortness of breath (dyspnea) is a common symptom of pneumonia.
It occurs when the lungs are unable to provide enough oxygen to the body, leading to a feeling of breathlessness.
The ability to ambulate without shortness of breath suggests that the pneumonia has improved and that the lungs are functioning more effectively.
Nursing Test Bank
Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is C
Explanation
Choice A rationale:
Incorrect. The kidneys do play a role in acid-base balance, but they primarily eliminate acids other than carbon dioxide. They do not significantly convert carbon dioxide for elimination.
Elaboration: While the kidneys help regulate acid-base balance through reabsorption and excretion of bicarbonate and hydrogen ions, their role in carbon dioxide elimination is minimal. They primarily excrete acids like uric acid, phosphoric acid, and lactic acid.
Choice B rationale:
Incorrect. Hyperventilation would decrease carbon dioxide levels, not contribute to respiratory acidosis. Respiratory acidosis is characterized by elevated carbon dioxide levels.
Elaboration: Hyperventilation leads to rapid and excessive breathing, causing a decrease in carbon dioxide levels in the blood. This can result in respiratory alkalosis, not respiratory acidosis.
Choice C rationale:
Correct. Respiratory acidosis is caused by the accumulation of carbon dioxide in the blood. This can happen due to impaired ventilation, such as in conditions like chronic obstructive pulmonary disease (COPD), pneumonia, or respiratory failure.
Elaboration: Carbon dioxide is produced as a byproduct of cellular metabolism. It is normally removed from the body through exhalation. When ventilation is impaired, carbon dioxide cannot be efficiently eliminated, leading to its buildup in the blood. This excess carbon dioxide reacts with water to form carbonic acid, lowering blood pH and causing respiratory acidosis.
Choice D rationale:
Incorrect. Low blood oxygen levels (hypoxemia) can stimulate the respiratory rate, but this would not directly cause respiratory acidosis. It might lead to hyperventilation, which could potentially cause respiratory alkalosis.
Elaboration: The body's respiratory center in the brainstem regulates breathing based on blood oxygen and carbon dioxide levels. Hypoxemia triggers a compensatory increase in respiratory rate to enhance oxygen intake. However, this response does not directly contribute to respiratory acidosis.
Correct Answer is A
Explanation
Choice A rationale:
Lactulose is a non-absorbable disaccharide that is metabolized by bacteria in the colon to produce lactic acid and acetic acid. These acids acidify the colon, which traps ammonia (NH3) in the colon and converts it to ammonium (NH4+). Ammonium is not absorbed by the colon and is excreted in the stool. This ammonia-lowering effect is the primary mechanism by which lactulose improves mental status in patients with hepatic encephalopathy.
Hepatic encephalopathy is a neuropsychiatric syndrome that occurs in patients with severe liver disease. It is caused by the buildup of ammonia in the blood, which can cross the blood-brain barrier and cause cerebral edema and impaired brain function.
The clinical manifestations of hepatic encephalopathy range from mild confusion and personality changes to coma. Improved mental status is a key therapeutic goal in the treatment of hepatic encephalopathy.
Studies have shown that lactulose can improve mental status in patients with hepatic encephalopathy. A meta-analysis of 11 randomized controlled trials found that lactulose was associated with a significant improvement in mental status compared to placebo.
The improvement in mental status is typically seen within 24 to 48 hours of starting lactulose therapy.
Choice B rationale:
Increased urine output is not a direct therapeutic effect of lactulose. Lactulose can cause diarrhea, which can lead to increased urine output due to fluid loss. However, this is not the primary mechanism by which lactulose improves mental status in patients with hepatic encephalopathy.
Choice C rationale:
Reduction in the number of liquid stools is a common side effect of lactulose. However, it is not a therapeutic goal in the treatment of hepatic encephalopathy. The goal of lactulose therapy is to improve mental status by lowering ammonia levels in the blood.
Choice D rationale:
Ability to ambulate independently is not a direct therapeutic effect of lactulose. Lactulose can improve mental status, which may indirectly lead to improved ambulation in some patients. However, this is not the primary mechanism by which lactulose works.
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