A client has a chest tube connected to a closed water-seal drainage system with suction. Which equipment should the nurse always have available at the client's bedside?

A. Suction subglottic area above the ETT cuff before entering the ETT. While subglottic suctioning helps prevent ventilator-associated pneumonia (VAP) by removing pooled secretions, it does not directly improve oxygenation during deep endotracheal suctioning. The priority is to optimize oxygenation before and after suctioning.
B. Use the ventilator settings to stack breaths prior to suctioning. Pre-oxygenating the client by delivering additional breaths via the ventilator helps prevent hypoxia during suctioning. Closed suction systems momentarily interrupt airflow, which can lead to oxygen desaturation. Providing 100% FiO₂ for 30–60 seconds before suctioning helps ensure adequate oxygenation and reduces complications.
C. Rinse suction catheters with normal saline between each suction pass. Flushing the catheter keeps it clean and patent, but it does not enhance oxygenation. Normal saline instillation before suctioning is not recommended, as it can increase infection risk and worsen secretion mobilization.
D. Suction for 30 seconds with each pass of the suction catheter. Prolonged suctioning can cause severe hypoxia, bradycardia, and airway trauma. Suction passes should be limited to 10–15 seconds to minimize complications. If additional suctioning is needed, the client should be reoxygenated between passes.

A. Decreased cardiac output. Central venous pressure (CVP), also called right atrial pressure (RAP), reflects right ventricular preload and overall fluid status. An increasing CVP indicates fluid overload or impaired right ventricular function, both of which can lead to decreased cardiac output. Conditions such as right heart failure, pulmonary hypertension, or excessive fluid resuscitation can cause elevated CVP, reducing the heart’s ability to pump effectively and leading to poor systemic circulation.
B. Ineffective airway clearance. Airway clearance is not directly related to CVP measurements. While severe pulmonary conditions like ARDS or COPD can contribute to cardiac strain and right heart failure, the primary mechanism for rising CVP is cardiac dysfunction or fluid overload, not airway obstruction.
C. Ineffective peripheral tissue perfusion. Although decreased cardiac output can impair tissue perfusion, this choice is too broad. Increased CVP specifically reflects right-sided heart function and preload, making decreased cardiac output the more precise diagnosis related to the pathophysiologic mechanism.
D. Deficient fluid volume. A low CVP is associated with hypovolemia and fluid deficits, while an increasing CVP suggests fluid overload, heart failure, or venous congestion. Deficient fluid volume would cause a downward trend in CVP, not an increase.