An impaired fibrinolytic process has been demonstrated in patients infected with SARS-CoV-2, including those in severe or critical condition. Disruption of fibrinolysis leads to fibrin deposition, which exacerbates inflammation and fibrosis and damages the pulmonary surfactant. Numerous authors point out the different course of coagulopathy in patients with COVID-19. It is reported that they may have a state of secondary hyperfibrinolysis, which may explain, at least in part, the increased incidence of venous thromboembolism, even among those patients already receiving appropriate anticoagulant treatment. This raises the question of whether current guidelines for the prevention and treatment of embolic–thrombotic complications, among patients with severe COVID-19, are sufficient. Some studies show evidence of clinical improvement in patients who have received fibrinolytic therapy, beyond the current indications for its implementation.