Background: Nowadays, the new coronavirus-induced severe acute respiratory syndrome (COVID-19) outbreak was primarily stated in December 2019. Three months later, the Director-General of the World Health Organization, avowed the COVID-19 a global pandemic. Gathered evidence discloses that coagulation syndrome is repeatedly seen in COVID-19, and the incidence is higher in severe cases. The worsening lung functions and coagulopathy are some of the most significant poor prognostic criteria in the outcome of COVID-19. The pragmatic coagulopathy in patients hospitalized with COVID-19 (COVID-19 associated coagulopathy) is categorized by the increased level of D-dimer and fibrinogen/fibrin degradation products. They are interrelated with the severity of COVID-19. This elevation will aid the arrangement of the patients consistent with the disease severity and management. These coagulation parameters elevation can point to a poor prognosis. Coagulopathy in COVID-19 mainly affects immobilized patients, those in critical care units, and those who have extra risk factors that predispose to coagulopathy, for instance, acute inflammatory conditions and hypoxia. The exact pathogenesis of hypercoagulability in COVID-19 is unwell understood. The signs suggest that the COVID‐19 coagulopathy is an evolving phenomenon in which endothelial damage, platelet aggregation, augmented innate immune response, and other measures as systemic inflammation favoring coagulation would divide up the severity of this disease. Understanding the pathophysiology of COVID-19 related coagulopathy is crucial for suitable treatment and monitoring of these patients. Encouraging interest in the potential uses of anticoagulation in COVID-19 particularly is the use of heparin that has a potential benefit over other anticoagulants due to its anticoagulant role, anti-inflammatory, and potentially anti-viral properties.