Pathophysiology of ARDS

Clinical lung injury

Alveolar epithelial damage

Predisposing factors:

Aspiration of gastric contents

Sepsis

Burns

Trauma

Inhalation of toxic chemicals

Endothelial damage

Platelet aggregation

Complement (C5a) activation

Initiation of inflammatory-immune response

Release of neutrophil chemotactic factors

Neutrophil aggregation & release of mediators:

Oxygen radicals, proteolytic enzymes, Arachidonic acid metabolites, PAF

Alveolocapillary membrane permeability

Alveolar capilliary leak

Exudation of fluid, protein, RBC’s into interstitium

Pulmonary edema & hemorrhage w/ severe impairment of alveolar ventilation

Bacterial endotoxin

Macrophage mobilization

Release of cytokines

vasoconstriction

Decrease flow

Impaired gas exchange

hypoxemia

Type II pneumocyte damage

Increase capilliary membrane permiability

Extravasation of fluid

Decrease surfactant production

Alveolar collapse

Atelectasis & impaired lung complianceDyspnea

& tachypne

a

Right to left shunt, hyaline membrane formation, finally fibrosis

Acute respiratory failure