Etiology and Pathophysiology
In a healthy individual, the process of gas exchange should take place efficiently and effectively with little effort by the individual. The gas exchange involves the intake of oxygen from the atmosphere via inhalation and the removal of carbon dioxide via exhalation. The process of inhalation starts in the neurons of the brain, which sense the need to exchange gases. The neurons signal the skeletal muscles in the diaphragm to contract and initiate inhalation. Once the air is inhaled, it will be conducted through the upper and lower airways deep into the respiratory tract to the alveoli, which are the terminal air spaces. Each adult has approximately 300 million alveoli to facilitate the gas exchange process (Grossman & Porth, 2014; Wilkinson, Treas, Barnett, & Smith, 2016).
The alveoli consist of two different types: type I and type II alveolar cells. Type I cells are thin squamous cells that make up 95% of the surface area and are unable to complete cell division. Type II cells are equally as numerous as type I cells, but they only contribute about 5% of the surface area. It is within these cells that surfactant is produced, which decreases the surface tension. When the surface tension is at an average level, it allows for more natural lung expansion during inhalation. Surfactant produced by type II cells is also a part of the immune regulation within the lungs (Grossman & Porth, 2014).
Conditions that lead to the development of ARDS can be direct or indirect. If the injury does not directly involve the lungs, an inflammatory response is triggered that spreads to the lungs. Because both direct and indirect injuries result in inflammation, the symptoms are similar. The inflammation impacts the alveolar-capillary membrane, which is impermeable except to very small molecules in healthy patients. Due to the inflammation, the membrane allows larger molecules to pass through and enter the alveoli, including debris, fluid, and proteins (Grossman & Porth, 2014; Ignatavicius et al., 2018; NHLBI, 2019).
As fluid enters the alveoli, which are typically dry, the ARDS patient accumulates more fluid and proteins in the lung than usual. This shift of fluid from the intravascular space into the alveoli impedes surfactant production, which is necessary to facilitate decreased surface tension resulting in more natural contraction and relaxation of the alveolar space. This also allows a hyaline membrane to form, which becomes resistant to gas exchange. As these changes occur, the patient will start to have trouble breathing which will worsen as the lung tissue stiffens allowing for decreased ability to inflate the lungs properly (Grossman & Porth, 2014; Ignatavicius et al., 2018).
These changes lead to impaired gas exchange resulting in refractory hypoxemia that does not resolve even with high levels of supplemental oxygen. One role of surfactant is to help the alveoli retain their shape and ability to remain open. Therefore, the alveoli will begin to collapse without a sufficient amount of surfactant resulting in further impaired gas exchange and eventually the total sum of the damage and dysfunction leads to fibrosis (Grossman & Porth, 2014; Ignatavicius et al., 2018).
The exact etiology of ARDS is not clear; however, an inflammatory response both at the local level and the systemic level does occur. Patients who develop ARDS frequently have another disorder already in progress and typically one that is causing a capillary leak in another part of the body, such as in pancreatitis. It is understood that neutrophils play an active role in ARDS and are present early in the disease. Because the neutrophils are highly active in ARDS, they are releasing products into the bloodstream that further perpetuate an inflammatory response (Grossman & Porth, 2014; Ignatavicius et al., 2018).