Pathophysiology of ARDS

Predisposing factors:
Aspiration of gastric contents Sepsis Burns Trauma Inhalation of toxic chemicals Type II pneumocyte damage

Clinical lung injury

Alveolar epithelial damage

Endothelial damage

Initiation of inflamm atoryimmune response

Comple ment (C5a) activati on

Increase capilliary membrane permiability Platelet aggregat ion Extravasation of fluid

Bacteri al endoto xin

Decrease surfactant production

Release of neutrophil chemotactic factors

Macroph age mobilizati on

Neutrophil aggregation & release of mediators: Alveolar collapse Oxygen radicals, proteolytic enzymes, Arachidonic acid metabolites, PAF

Release of cytokines

Dyspnea & tachypne a

Atelectasis & impaired lung compliance Alveolocapillary membrane permeability Right to left shunt, hyaline membrane formation, finally fibrosis

vasocons triction

Decrease flow Alveolar capilliary leak Impaired gas exchange

Acute respiratory failure

Exudation of fluid, protein, RBCs into interstitium

hypoxe mia Pulmonary edema & hemorrhage w/ severe impairment of alveolar ventilation