A client who had gastric bypass surgery 3 days ago is admitted to the intensive care unit (ICU) with shortness of breath and chest pain. The client has a 100% nonrebreather mask with an oxygen saturation of 88%. Which intervention should the nurse implement?

A. Administer famotidine 20 mg IV. Famotidine is a histamine-2 receptor antagonist used for stress ulcer prophylaxis in critically ill patients. While this medication may be beneficial, it is not the priority intervention based on the insulin protocol and the client's blood glucose level.
B. Titrate insulin infusion by 1 unit/hour. The client’s blood glucose is 160 mg/dL, which falls within the 150–199 mg/dL range according to the insulin protocol. The protocol directs the nurse to increase the insulin drip rate by 1 unit/hour to maintain blood glucose levels below 150 mg/dL. This is the most immediate and appropriate action.
C. Increase dopamine 2 mcg/kg. The client’s MAP is 66 mmHg, which meets the protocol goal of keeping MAP >65 mmHg. There is no indication for increasing dopamine at this time, as the blood pressure is already within the target range.
D. Raise oxygen by 10 percent. The client is on 50% FiO₂ via a face mask with an oxygen saturation of 92%, which is adequate oxygenation for a critically ill patient. Increasing FiO₂ unnecessarily may contribute to oxygen toxicity and is not required based on current oxygenation status.

• 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.