Acute respiratory distress syndrome (ARDS) is a syndrome of acute pulmonary insufficiency that occurs in response to local or systemic tissue hypoxia, ischemia and reperfusion, with a multifactorial etiology. The cause of ARDS can be a variety of factors, from viruses and bacteria to injuries and intoxications.
The inflammatory process in the lungs is associated with complex immunological reactions: activation of neutrophils, endothelial cells, production of free oxygen radicals. The main role in ARDS pathogenesis is played by pulmonary edema due to damage to the alveolar-capillary membrane. Excessive immune activation in response to a damaging agent (with massive cytokine release and the development of a “cytokine storm”) is probably as dangerous as immune deficiency, only with a different pathogenetic mechanism and consequences.
After recovery from ARDS, there are unpleasant consequences in the form of pulmonary insufficiency of varying severity due to pulmonary fibrosis (consolidation of lung tissue that occurs at the site of previous inflammatory changes, scarring). This condition is described by patients as frequent shortness of breath, even with light exercise, fatigue, inability to breathe “to the full breast”. Decreased effective respiratory function of the lungs leads to hypoxia of body tissues, which in turn disrupts all body systems, especially cardiovascular and nervous.