Question

The next day, the nurse notices that Mr. T has marked hypoxemia, which is not responding to increased levels of oxygen. A chest x-ray is obtained, which reveals diffuse bilateral infiltrates. He is diagnosed with ALI/ARDS. 6. What is the pathophysiology associated with ALI/ARDS (provide a specific process, start to finish)?

Answer 1

The ARDS stands for the acute respiratory distress syndrome, which is a life threatening lung condition. It prevents the transfer of the oxygen from the lung to the blood, hence, causing hypoxemia.

As given in the question, the patient has a infiltrate in the lungs, which is preventing the transfer of oxygen from the lung to the blood. This condition can be caused due to inflammation and pulmonary edema.

The inflammation is a defense mechanism of the body that helps the body to fight against the things causing harm to it. The ALI of the patient causes the inflammation and lead to the inflammatory responses. The inflammatory responses are mainly triggered by the cytokines and white blood cells.

The pulmonary edema is caused by the retention of the fluids in the alveolar sacs, which is transferred from the blood vessels to the lungs. This fluid can form a barrier at the alveolar lining and blocks the gas exchange in the lungs, resulting in oxidative stress.

The fluid present in the lungs contains neutrophils, proinflammatory cytokines as well as the biomarkers for the oxidative stress. This fluid causes prolonged blood-gas barrier, which may result in the pulmonary-parenchymal inflammation.

Also, fluid retention causes the activation of the repair mechanism. In this process, the precipitated protein is cleared by the macrophage-driven alveolar cleaning with tumor necrosis factors, which may lead to increased inflammatory activity.

On the other hand, the above activity can cause mechanical stress on the pulmonary microcirculation, which causes the activation of several intracellular signalling pathways. this activation of the intracellular pathways further increases the inflammatory cytokine production, macrophage activation, and acute inflammation. Along with this, the oxidative stress caused by the blood-gas barrier compromise activates the redox-sensitive pathways causing more inflammation and apoptosis.

Hence, the pulmonary edema can lead to an inflammatory response. The inflammatory responses and the oxidative stress caused by the pulmonary edema may further lead to more damage to the alveolar-capillary barrier and more fluid retention in the lungs.

So, the pathophysiology can be represented as below:

ALI àInflammation àretention of fluid in the lungsàpulmonary edemaàblood gas barrieràhypoxemia.