What is the primary mechanism by which positive end-expiratory pressure (PEEP) improves oxygenation in patients with acute respiratory distress syndrome (ARDS)?

The primary mechanism by which positive end-expiratory pressure (PEEP) improves oxygenation in patients with acute respiratory distress syndrome (ARDS) is by increasing the functional residual capacity (FRC) and preventing alveolar collapse at the end of expiration. ARDS is a severe lung injury characterized by widespread inflammation, pulmonary edema (fluid in the lungs), and alveolar collapse. This collapse results in reduced lung volume and significant intrapulmonary shunting, where blood passes through the lungs without participating in gas exchange, leading to hypoxemia (low blood oxygen levels). PEEP is the application of positive pressure in the airway at the end of exhalation during mechanical ventilation. By maintaining a positive pressure, PEEP prevents the alveoli from collapsing completely. This increases the FRC, which is the volume of air remaining in the lungs after a normal exhalation. The increase in FRC caused by PEEP does several things: it reopens previously collapsed alveoli, it increases the surface area available for gas exchange, and it reduces shunting. With more alveoli open and participating in gas exchange, a greater proportion of the blood passing through the lungs can pick up oxygen, thereby improving oxygenation and reducing the severity of hypoxemia. While PEEP can improve oxygenation, it's crucial to note that excessive PEEP can lead to alveolar overdistension and decreased cardiac output, so it must be carefully titrated based on the patient's response.