Acute Respiratory Distress

Syndrome (ARDS)
(Lungs; Alveoli)

Modifiable Risk Non-Modifiable

ETIOLOGICAL
Factors CAUSE Risk Factor
“Unknown”

 Bacteremia  Genetic factors

 Sepsis (FAS gene and ALI
Increase in the permeability
 Trauma with and without susceptibility)
of the alveolar-capillary
pulmonary contusion barrier
 Fractures particularly
multiple fractures and
long bone fractures
 Burns
 Massive transfusion
 Pneumonia Diffuse alveolar damage (DAD)
 Aspiration and lung endothelial injury
 Drug overdose
 Near drowning
 Post-perfusion injury
 After cardiopulmonary
bypass
Influx of fluid into the alveoli
 Pancreatitis
 Fat embolism
 Damage either to the vascular
endothelium or to alveolar
epithelium

Vascular Endothelium Alveolar Epithelium

(ex: Sepsis) (Ex: Aspiration of Gastric Contents)

Increase capillary
permeability and the influx of Promotes Pulmonary
protein-rich fluid into the Edema Formation
alveolar space

Damaged to type 1 cells allow both Damaged to Type 2 cells results in

increased entry of fluid into the decreased production of surfactant
alveoli and decreased clearance with resultant decreased compliance
fluid from the alveolar space and alveolar collapse

Decrease Lung Compliance
Type I cells, which
makes up 90% of the
alveolar epithelium,
are injured easily.
Type II alveolar
Pulmonary epithelial cells are
hypertension relatively more
resistant to injury.
However, type II cell
have several
Impairment in Gas Exchange important functions,
including the
production of
surfactant, ion
transport, and
proliferation and
Acute Respiratory Distress differentiation into
Syndrome (ARDS) type I cells after
cellular injury.

Signs and
Symptoms