 So let's look at physiologically what is going on. So over here we have the normal pulmonary capillary alveolar structure. So we have the pulmonary artery that goes down into the pulmonary capillaries, CO2 diffuses into the alveolus, O2 diffuses into the pulmonary vein, and then the oxygenated blood gets carried to the body and the cells. Now what happens in ARDS, there is an injury to this alveolar capillary membrane. Whenever an injury occurs, for any of these reasons up here, the immune system is triggered and this cascade of immune cells want to come and help fight whatever is the cause of the problem. So there's this cascade of cellular and biochemical changes that triggers these immune cells that are usually well intended, such as neutrophils, macrophages, lymphocytes, monocytes, and all of those produce cytokines. Cytokines are basically cells that help promote the immune system to do its job. Especially with COVID, you have probably heard of the term cytokines stored. So now we have this massive immune response, all these cells that want to come fight any of these causes, and therefore, in order for these mediators to be released from the pulmonary capillaries, this permeability has to be opening up. So they have to all be released and what happens when the cells are released, they're released in fluid. And so then we have this interstitial edema that occurs between the alveolus and the pulmonary capillaries. So this increased fluid that happens here. And then if we have basically this alveolus that's now covered in fluid, it's not going to be able to perform the oxygen and CO2 exchange as a normal alveolus would. Now this increased vascular permeability causes the interstitial edema. And then the lungs get kind of stiff because they lose their compliance, their ability to open and contract as the chest wall expands and then recoils. And then platelets also come to play. They aggregate and release more chemical mediators, which then means that more cells are being attracted to the alveolar capillary membrane and the fluid crosses that membrane. And as you can see here, this alveolus is swollen, it's very puffy. And now that fluid level is just increasing here. So basically this alveolus you could think of is drowning in this fluid that all these chemical mediators from the immune system are causing. And this alveolar edema then does not allow for the oxygen and CO2 exchange and therefore the patient is going to have this acute respiratory distress syndrome.