Scribd
Upload
3K views1 page

Pathophysiology ARDS

The document summarizes the pathophysiology of acute respiratory distress syndrome (ARDS). It outlines predisposing factors like sepsis, burns, and aspiration that can cause alveolar epithelial and endothelial damage, initiating an inflammatory response. This leads to increased capillary permeability, surfactant dysfunction, and neutrophil aggregation—releasing oxidative and proteolytic mediators that cause alveolar collapse and impaired gas exchange, resulting in acute respiratory failure.

Uploaded by

Roderick Agbuya
Copyright
© Attribution Non-Commercial (BY-NC)
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as DOCX, PDF, TXT or read online on Scribd
3K views1 page

Pathophysiology ARDS

The document summarizes the pathophysiology of acute respiratory distress syndrome (ARDS). It outlines predisposing factors like sepsis, burns, and aspiration that can cause alveolar epithelial and endothelial damage, initiating an inflammatory response. This leads to increased capillary permeability, surfactant dysfunction, and neutrophil aggregation—releasing oxidative and proteolytic mediators that cause alveolar collapse and impaired gas exchange, resulting in acute respiratory failure.

Uploaded by

Roderick Agbuya
Copyright
© Attribution Non-Commercial (BY-NC)
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as DOCX, PDF, TXT or read online on Scribd
You are on page 1/ 1

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

You might also like