A client who is admitted to the emergency department (ED) following a motorcycle collision is having difficulty breathing. While assessing the client's chest and lungs, the nurse notes that there are no breath sounds over the left lung fields. Which action(s) should the nurse implement? Select all that apply.

A. Promote oxygenation to tissues. Oxygenation is not a primary goal in DKA management unless there is a coexisting condition causing hypoxia. DKA primarily leads to metabolic acidosis and dehydration rather than respiratory failure, and oxygenation is typically maintained unless complications such as pneumonia or severe shock develop.
B. Reverse dehydration. Severe dehydration occurs in DKA due to osmotic diuresis caused by hyperglycemia. The priority is to restore intravascular volume with isotonic IV fluids such as 0.9% normal saline to improve circulation, support kidney function, and prevent shock. Fluid replacement is essential for stabilizing blood pressure and promoting glucose clearance.
C. Replace insulin. The lack of insulin is the primary cause of DKA, leading to unchecked lipolysis and ketone production. IV insulin therapy is necessary to suppress ketogenesis, lower blood glucose levels, and allow cells to use glucose for energy. Insulin must be administered cautiously with continuous monitoring to prevent hypoglycemia and electrolyte imbalances.
D. Correct electrolytes that are out of normal range. Electrolyte imbalances, particularly potassium depletion, are common in DKA due to osmotic losses and shifting caused by insulin therapy. Potassium replacement is required even if levels appear normal initially, as insulin will drive potassium into cells, leading to hypokalemia. Sodium and bicarbonate levels should also be monitored and corrected as needed.
E. Provide respiratory support. Respiratory support is not typically required unless the client experiences severe respiratory distress or altered mental status. Kussmaul respirations are a natural compensatory mechanism that helps the body exhale CO₂ and correct acidosis. Supplemental oxygen is only necessary if there is an underlying pulmonary condition or respiratory failure.
F. Prevent hyperventilation. Hyperventilation in the form of Kussmaul respirations is the body's way of compensating for metabolic acidosis. It should not be suppressed, as it plays a crucial role in reducing acid buildup. Treating the underlying cause of DKA with fluids, insulin, and electrolyte replacement will allow respiratory function to normalize.

• 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.