A nurse is caring for a client immediately following endotracheal intubation. The nurse should assess the client for complications by performing which of the following priority action?

Pulmonary Function Tests assess chronic respiratory conditions like COPD and asthma. In an acute pneumothorax, these tests are unnecessary as the priority is stabilizing the airway and restoring lung expansion. The client is in respiratory distress, making PFTs impractical and irrelevant at this stage.

Obtain Intravenous Access: IV access is necessary to administer fluids, medications, and potential emergency interventions. Given the client's signs of respiratory distress and hemodynamic instability (tachycardia, hypotension), IV access ensures rapid treatment in case of deterioration.

Thoracentesis: Thoracentesis is used to remove pleural fluid in conditions like pleural effusion but is not appropriate for a pneumothorax. Inserting a needle into the pleural space could worsen the lung collapse and lead to further respiratory compromise. The correct intervention is a chest tube insertion.

Obtain ABGs: ABGs provide critical information on oxygenation, ventilation, and acid-base balance. The client has tachypnea, cyanosis, and low O₂ saturation, indicating possible respiratory acidosis or hypoxemia. ABGs will guide oxygen therapy and further management.

Prepare for Insertion of a Chest Tube: A chest tube is the definitive treatment for a pneumothorax. It removes air from the pleural space, allowing lung re-expansion. Given the client's absent breath sounds, tachypnea, and hypoxia, immediate chest tube insertion is necessary to prevent further deterioration.

Computed Tomography (CT) of the Chest: While a CT scan provides detailed lung imaging, it is not the first-line diagnostic tool for pneumothorax. A chest X-ray is usually sufficient to confirm the diagnosis. In an emergency setting, immediate intervention (such as chest tube placement) takes priority over advanced imaging.

A. Increased arterial oxygen: Clients with COPD typically experience chronic hypoxemia due to alveolar destruction, airway inflammation, and mucus production, which impair gas exchange. Rather than increased oxygen levels, they often have a decreased PaO₂, requiring supplemental oxygen therapy. However, excessive oxygen administration can suppress their respiratory drive, worsening CO₂ retention.
B. Increased pH: COPD is associated with respiratory acidosis due to chronic CO₂ retention from inadequate alveolar ventilation. While the kidneys compensate by increasing bicarbonate retention, the pH usually remains low or near normal in chronic cases rather than becoming elevated. A higher pH would indicate alkalosis, which is not typical in COPD unless there is an additional metabolic disturbance.
C. Increased carbon dioxide: COPD causes airway obstruction and reduced alveolar ventilation, leading to CO₂ retention (hypercapnia). As CO₂ accumulates in the blood, it lowers the pH, resulting in respiratory acidosis. Chronic hypercapnia is a hallmark of advanced COPD, and in response, the kidneys retain bicarbonate to partially compensate, stabilizing the pH over time but leaving PaCO₂ elevated.
D. Decreased alveolar function: While COPD does lead to progressive alveolar damage and reduced gas exchange, this is a structural and functional change rather than a specific abnormality seen in arterial blood gases. The primary ABG finding in COPD is hypercapnia, which reflects inadequate ventilation and CO₂ retention rather than just decreased alveolar function alone.