A client admitted to the intensive care unit (ICU) with acute respiratory distress syndrome (ARDS) is intubated and placed on assist-control mechanical ventilation. When suctioning pulmonary secretions from the endotracheal tube (ETT) using a closed suction system, which action should the nurse implement to ensure that the client receives adequate oxygenation?

A. Insert a large bore peripheral IV catheter. The client is showing signs of shock (tachycardia, hypotension, tachypnea) likely due to envenomation and systemic venom effects. Rapid IV access is essential for fluid resuscitation, administration of antivenom, and management of shock. A large bore (18-gauge or larger) IV catheter allows for aggressive fluid therapy to maintain perfusion and prevent circulatory collapse.
B. Raise extremity above the heart. Elevating the limb can increase venom circulation, worsening systemic effects. Instead, the affected extremity should be kept at heart level to slow venom spread while ensuring adequate perfusion.
C. Tighten the cloth around the leg. Further tightening the makeshift tourniquet can lead to vascular compromise, ischemia, and increased local tissue damage. Modern guidelines discourage tourniquets as they do not prevent venom spread effectively and may worsen outcomes. The best approach is to loosen or remove restrictive bindings and keep the limb immobilized at heart level.
D. Apply ice over the bite mark. Cold therapy is contraindicated as it can worsen tissue damage by causing vasoconstriction, trapping venom, and increasing necrosis. Instead, the priority is IV access, fluid resuscitation, and preparing for possible antivenom administration.

• 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.