In normal pregnancy, the cardiac output increases and peripheral resistance decreases with increasing gestational age. It is generally believed that cardiac output begins to increase at 8 to 10 weeks of pregnancy, and reaches a peak at 32 to 34 weeks of pregnancy, which is 30% to 45% higher than that in non-pregnancy, and maintains this level until delivery. The decrease of peripheral vascular resistance reduces the arterial pressure, and the diastolic blood pressure decreases significantly, and the pulse pressure difference widens. From 6 to 10 weeks of gestation, the blood volume of pregnant women increases with the increase of gestational age, and increases by about 40% at the end of pregnancy, but the increase of plasma volume far exceeds the number of red blood cells, plasma increases by 40% to 50%, and red blood cells increases by 10% to 15%. Therefore, in normal pregnancy, the blood is diluted, manifested as decreased blood viscosity, decreased hematocrit, and increased erythrocyte sedimentation rate [1].

Blood coagulation factors Ⅱ, Ⅴ, VII, Ⅷ, IX, and Ⅹ all increase during pregnancy, and can reach 1.5 to 2.0 times of normal in the middle and late pregnancy, and the activities of coagulation factors Ⅺ and  decrease. Fibrinopeptide A, fibrinopeptide B, thrombinogen, platelet factor Ⅳ and fibrinogen increased significantly, while antithrombin Ⅲ and protein C and protein S decreased. During pregnancy, the prothrombin time and activated partial prothrombin time are shortened, and the plasma fibrinogen content increases significantly, which can increase to 4-6 g/L in the third trimester, which is about 50% higher than that in the non-pregnant period. In addition, plasminogen increased, euglobulin dissolution time was prolonged, and coagulation-anticoagulation changes made the body in a hypercoagulable state, which was beneficial to effective hemostasis after placental abruption during labor. In addition, other hypercoagulable factors during pregnancy include the increase of total cholesterol, phospholipids and triacylglycerols in the blood, androgen and progesterone secreted by the placenta reduce the effect of certain blood coagulation inhibitors, placenta, uterine decidua and embryos. The presence of thromboplastin substances, etc., can promote the blood to be in a hypercoagulable state, and this change is exacerbated with the increase of gestational age. Moderate hypercoagulation is a physiological protective measure, which is beneficial to maintain fibrin deposition in arteries, uterine wall and placental villi, help maintain the integrity of the placenta and form thrombus due to stripping, and facilitate rapid hemostasis during and after delivery. , is an important mechanism to prevent postpartum hemorrhage. At the same time of coagulation, secondary fibrinolytic activity also begins to remove thrombus in the uterine spiral arteries and venous sinuses and accelerate the regeneration and repair of the endometrium [2].

However, a hypercoagulable state can also cause many obstetric complications. In recent years, studies have found that many pregnant women are prone to thrombosis. This disease state of thromboembolism in pregnant women due to genetic defects or acquired risk factors such as anticoagulant proteins, coagulation factors, and fibrinolytic proteins is called thrombosis. (thrombophilia), also known as the prothrombotic state. This prothrombotic state does not necessarily lead to thrombotic disease, but may lead to adverse pregnancy outcomes due to imbalances in coagulation-anticoagulation mechanisms or fibrinolytic activity, microthrombosis of uterine spiral arteries or villus, resulting in poor placental perfusion or even infarction, such as Preeclampsia, placental abruption, placental infarction, disseminated intravascular coagulation (DIC), fetal growth restriction, recurrent miscarriage, stillbirth and premature birth, etc., can lead to maternal and perinatal death in severe cases.