ARDS

Disease / Phenomenon

Acute respiratory distress syndrome (ARDS) is a rapidly developing form of respiratory failure in which the lungs fill with inflammatory fluid and can no longer oxygenate blood effectively. It is not a primary lung disease but a stereotyped injury response triggered by something else: pneumonia, sepsis, aspiration, severe trauma, pancreatitis, burns, or major transfusion. Within hours to days, patients become severely short of breath, oxygen levels fall despite supplemental oxygen, and chest imaging shows diffuse bilateral opacities that are not explained by heart failure alone. Severity is graded by the ratio of arterial oxygen to inspired oxygen, and management centers on treating the underlying cause while supporting gas exchange with lung-protective ventilation.

The underlying injury is damage to the alveolar-capillary barrier. Activated neutrophils and macrophages release cytokines, proteases, and reactive oxygen species; endothelial and epithelial tight junctions loosen; and protein-rich edema floods the alveoli, inactivating surfactant and collapsing gas-exchange units. Coagulation activation produces microthrombi, and in surviving patients a fibroproliferative phase may deposit collagen and leave lasting lung stiffness. Key mediators include IL-6, IL-8, TNF-alpha, and NF-kB-driven signaling. This page separates ARDS into its biological processes, the molecular pathways inside each, and their measurable biomarkers.