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The lung tissue contains various hemostatic system elements, which can be released from the lungs, both under physiological and pathological conditions. The COVID-19 pandemic has led to an increase in the number of patients with acute respiratory distress syndrome (ARDS) in intensive care units worldwide. When the lungs are damaged, coagulation disorders are mediated by tissue factor (TF) - factor VIIa (F VIIa), and inhibition of this pathway completely eliminates intrapulmonary fibrin deposition. A tissue factor pathway inhibitor TFPI also contributes to pulmonary coagulationdisturbance in ARDS. Pulmonary coagulationdisturbance caused by pneumonia can worsen the damage to the lungs and thus contribute to the progression of the disease. Cytokines are the main linking factors between inflammation and changes in blood clotting and fibrinolysis. The sources of proinflammatory cytokines in the lungs are probably alveolar macrophages. The activation of alveolar macrophages occurs through the nuclear factor kappa-bi (NF-κB), which controls thetranscription of the expression of immune response genes, cell apoptosis, which leads to the development of inflammation and autoimmune diseases as a result of direct stimulation of TF activation. Conversely,coagulation itself can affect bronchoalveolar inflammation. Coagulation leads to the formation of proteases that interact with specific cellular receptors, activating intracellular signaling pathways. The use of anticoagulant therapy, which also has an anti-inflammatory effect, perhaps one of the therapeutic targets for coronavirus infection.The difficulty here is that it seems appropriate to study anticoagulant interventions’ influence on clinically significant cardio-respiratory parameters.

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