What is the mechanism of hypoxemia in ARDS?

The mechanism of hypoxemia in ARDS is primarily attributed to ventilation-perfusion mismatch and shunting. In ARDS, there is an inflammatory process that disrupts the alveolar-capillary membrane, leading to increased permeability. This results in pulmonary edema, atelectasis, and impaired gas exchange.

In a healthy lung, ventilation (air reaching the alveoli) and perfusion (blood flow in the pulmonary capillaries) are matched to optimize oxygenation. However, in ARDS, the presence of fluid in the alveoli and the collapse of lung units contribute to areas where alveoli are not adequately ventilated but still receive blood flow. This mismatch between ventilation and perfusion means that even though blood is flowing through the lungs, it is not being efficiently oxygenated, leading to hypoxemia.

Additionally, some of the blood flow may pass through areas of the lung that are non-ventilated, effectively shunting deoxygenated blood into the systemic circulation without participating in gas exchange. This results in a lower overall partial pressure of oxygen in the arterial blood, contributing significantly to hypoxemia observed in patients with ARDS.

Understanding this mechanism is crucial for managing ARDS effectively, as treatments often aim to improve ventilation-perfusion matching