Pathways and Pathophysiology of Acute Respiratory Distress Syndrome (ARDS)


Acute Respiratory Distress Syndrome (ARDS) is the total lung damage due to various etiologies. This condition can be triggered by many things, such as sepsis, viral or bacterial pneumonia, aspiration of gastric contents, chest trauma, prolonged shock, burns, fat embolism, drowning, massive blood transfusion, cardiopulmonary bypass, O2 toxicity, bleeding acute pancreatitis, gas inhalation toxic, as well as the consumption of certain drugs. "ADRs is a medical emergency that is triggered by a variety of acute processes that relate directly or indirectly to the lung damage.


Pathophysiology of Acute Respiratory Distress Syndrome (ARDS)

Pathophysiology of ARDS can be explained as follows:
Systemic damage caused decreased tissue perfusion and cellular hypoxia resulting in the release of biochemical factors (lysosomal enzymes, vasoactive, the complement system, metabolic acid, collagen, histamine) that cause an increase in pulmonary capillary permeability, which causes a decline in the activity of the surfactant resulting in interstitial edema alveolar lung and causes progressive alveolar collapse that decreased lung compliance (stiff lung) and increases arterial shunting resulting in hypoxia.

Lung fluid movement in the case of ARDS:
  • Occurs stretching / deposition of hyaline membranes.
  • Epithelial wide intra-alveolar junction.
  • Interstitial edema, intravascular fluid out, in and out of the protein into the alveoli.
  • Pulmonary capillary endothelial rupture.
  • Erythrocytes out of the intravascular into the lungs causes the phenomenon frozzy sputum.


Pathways of Acute Respiratory Distress Syndrome (ARDS)

Systemic Damage -> Decreased tissue perfusion -> cellular hypoxia -> Release of biochemical factors (lysosomal enzymes, vasoactive, the complement system, metabolic acid, collagen, histamine) -> Increased pulmonary capillary permeability -> Decreased surfactant activity -> alveolar interstitial pulmonary edema -> progressive alveolar collapse -> Decrease in lung compliance (Stiff lung) -> Increased shunting -> arterial hypoxia.