In this article, we will discuss the Pathophysiology of Acute Respiratory Distress Syndrome. So, let’s get started.
ARDS can be considered as the earliest manifestation of a generalized inflammatory reaction and irrespective of its cause, evolves through the following phases:
Exudative phase (noncardiogenic pulmonary edema): This is the early phase of a ARDS; occurs within 24-96 hours following a precipitating event. It is characterized by endothelial injury, denudation of type I epithelial cells, increase in vascular permeability, release of inflammatory cytokines and hyaline membrane formation. There is decreased surfactant production. It usually lasts for 3-7 days. The clinical hallmarks of this phase are bilateral pulmonary infiltrates (noncardiogenic pulmonary edema), dyspnea and marked hypoxemia.
Proliferative phase (stage of development of pulmonary hypertension): By 3-7 days patient who survived the initial phase progresses to proliferative stage. Necrotic Type I cells are replaced by type II epithelial cells which proliferate and form new alveolar epithelium. Interstitial and alveolar edema starts decreasing and these spaces are filled with RBCs, inflammatory cells and cellular debris. This phase is characterized by worsening hypoxemia (cyanosis) as a result of pulmonary shunting of blood and development of pulmonary hypertension as a result of vasoconstructive response and microthrombi formation.
Fibrotic phase: After about 7-10 days of onset of ARDS, activated fibroblasts accumulate in the interstitial spaces. Subsequently fibrosis sets in with loss of elastic tissue and obliteration of the lung vasculature. This may slowly resolve or may result in lung destruction which may be irreversible.