Which condition is defined as collapse of part or all of a lung, so that gas exchange is lost in the affected area?

Atelectasis is collapse of a portion of the lung so that gas exchange cannot occur; airway obstruction, such as from a mucus plug, is a leading cause.

Rationale

The condition described is atelectasis. Atelectasis refers to a state in which part or all of the lung fails to expand fully and collapses. The other options each reflect a distinctly different pathophysiology and must be clearly differentiated. Pneumonia is inflammation of the lung parenchyma caused by an infectious pathogen, and bronchitis is inflammation of the bronchial mucosa. Pulmonary edema is abnormal accumulation of fluid in the pulmonary interstitium or alveoli, and pleurisy refers to inflammation of the pleura.

Pathophysiology and Mechanisms

Atelectasis is broadly classified by mechanism as obstructive or non-obstructive. The supporting literature^[1] describes right middle lobe syndrome (RMLS) and specifies that chronic atelectasis arises from either obstructive or non-obstructive mechanisms.

Obstructive atelectasis occurs when the airway is blocked by intrinsic or extrinsic factors. As in the case reported in the literature^[1], when a mucus plug occludes a bronchus, air in the alveoli distal to the obstruction is gradually absorbed into the bloodstream. Intra-alveolar pressure falls and the alveoli collapse, producing absorption atelectasis. The finding of persistent mucosal edema on bronchoscopy even after removal of the mucus plug suggests that inflammatory narrowing of the airway lumen can also contribute to atelectasis.

Non-obstructive atelectasis develops without direct airway blockage, resulting instead from changes in intrapleural pressure surrounding the lung or from impaired surfactant function. The supporting literature^[2] identifies reduced functional residual capacity (FRC), oxygen absorption, and surfactant dysfunction as reasons atelectasis commonly occurs in dogs after general anesthesia. General anesthesia and neuromuscular blockade reduce diaphragmatic tone and therefore FRC, so the alveoli can no longer remain adequately inflated at physiologic end-expiration and collapse easily. In addition, a high inspired oxygen concentration washes nitrogen out of the alveoli (denitrogenation); once oxygen is rapidly absorbed into the pulmonary capillaries, too little gas remains to support the alveoli, promoting absorption atelectasis. Impaired surfactant function raises alveolar surface tension and further accelerates alveolar collapse.

Clinical Application to Practice

The supporting literature^[2] demonstrates how ultrasound can be applied to the diagnosis and treatment of atelectasis. That study used the Lung Ultrasound Atelectasis Score (LUAS) to objectively grade the severity of atelectasis. It also evaluated therapeutic strategies including an alveolar recruitment maneuver (ARM) and application of incremental PEEP. An ARM temporarily applies elevated airway pressure to reopen collapsed alveoli. Stepwise increases in PEEP to identify the optimal level are then important to keep recruited alveoli from collapsing again at end-expiration. Because ultrasound-confirmed atelectasis was observed in both the mechanically ventilated and the spontaneously breathing groups, nurses must anticipate the risk of atelectasis and closely assess respiratory status even in spontaneously breathing patients in the PACU or ICU who are not receiving mechanical ventilation.

For the NCLEX, atelectasis goes beyond simple term recall and connects directly to nursing interventions that prevent postoperative complications. Encouraging deep breathing and coughing, early ambulation, and use of an incentive spirometer are all evidence-based measures that increase FRC and expand the alveoli to prevent atelectasis. For patients at risk of obstruction from mucus plugging, adequate hydration and humidification along with postural drainage to mobilize secretions are essential.