A client is brought to the emergency department (ED) following a motor vehicle collision with blunt trauma to the chest. Which finding should the nurse report immediately to the healthcare provider (HCP)?

• 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.

A. Temperature. While temperature monitoring is important in septic shock to assess infection control, it is not an indicator of dopamine's effectiveness. Dopamine primarily affects renal perfusion and blood pressure, not body temperature regulation.
B. Heart sounds. Dopamine is a vasopressor and inotropic agent, but it does not directly impact heart sounds. While it can increase myocardial contractility, assessing blood pressure and perfusion parameters is more relevant in evaluating its therapeutic effects.
C. Urinary output. Low-dose dopamine (1-5 mcg/kg/min) primarily acts as a dopaminergic agonist, increasing renal blood flow and urine output by dilating renal arteries. In septic shock, maintaining adequate kidney perfusion is critical to prevent acute kidney injury (AKI). A therapeutic response to dopamine would be seen as improved urinary output (≥ 30 mL/hr), indicating effective renal perfusion.
D. Pupil response. Dopamine does not directly affect pupil size or reactivity. Pupil assessment is more relevant in neurological evaluations, not in monitoring the effects of dopamine in septic shock.