Topic 9 — Atelectasis, Acute Lung Injury and Respiratory Distress Syndrome

Initiating Problem

Airway obstruction, external compression, fibrosis, acute lung injury or prematurity

→

Core Mechanism

Loss of alveolar air, impaired expansion, permeability edema or increased surface tension

→

Functional Change

Alveolar collapse, reduced compliance and impaired ventilation

→

Gas-Exchange Effect

Ventilation-perfusion disturbance and reduced oxygenation

→

Clinical Expression

Respiratory distress, tachypnea and impaired oxygenation when severe

→

Diagnostic / Treatment Link

Morphology or imaging identifies the process; respiratory support maintains gas exchange

Two closely related branches

ARDS:
acute inflammatory injury
→
endothelial and epithelial damage
→
protein-rich alveolar edema
→
diffuse alveolar damage and hyaline membranes.

Neonatal RDS:
prematurity
→
inadequate surfactant
→
increased surface tension
→
alveolar collapse and reduced compliance.

Atelectasis Mechanism Connection

Blocked bronchus → distal gas absorption → resorption atelectasis.

Pleural pressure or fibrosis → impaired expansion → compression or contraction atelectasis.

ARDS Morphology Connection

Alveolar-capillary injury → permeability edema → fibrin-rich material plus necrotic epithelial debris → hyaline membranes.

Neonatal RDS Recognition

Prematurity → surfactant deficiency → tachypnea, grunting and retractions.

Poor alveolar expansion → diffuse fine ground-glass appearance with air bronchograms.

Management Connection

Repeated alveolar collapse → CPAP maintains end-expiratory pressure → better alveolar stability.

Surfactant deficiency → exogenous surfactant → lower surface tension and improved compliance.

⭐ Bronchial obstruction → distal gas absorption → resorption atelectasis.

External pleural pressure → impaired expansion → compression atelectasis; fibrosis → mechanical restriction → contraction atelectasis.

⭐ Alveolar-capillary barrier injury → increased permeability → protein-rich pulmonary edema in ARDS.

⭐ Diffuse alveolar damage → fibrin-rich edema plus epithelial debris → hyaline membranes.

Type II pneumocyte injury in ARDS → reduced surfactant activity → alveolar instability; later proliferation of these cells supports epithelial repair.

⭐ Prematurity → inadequate surfactant → increased surface tension → alveolar collapse, reduced compliance and respiratory distress.

Respiratory distress plus diffuse poor aeration → pulse oximetry and blood gas assessment; chest radiography may show fine ground-glass change with air bronchograms.

CPAP → maintains alveolar expansion; exogenous surfactant → corrects the underlying surface-tension problem and improves lung compliance.