Patients with pulmonary embolism can be treated with thrombolysis, subsequent anticoagulation, or direct anticoagulation without thrombolysis, depending on the severity of their condition after admission. Thrombolysis, as the name implies, is the dissolution of the formed thrombus to allow the blood vessel to reopen. The patient’s acute symptoms will be relieved when the clot that blocked the blood vessel is dissolved. Fresh clots (formed less than 14 days ago) are more effective after thrombolysis, and the clot may be completely dissolved within a week to two weeks; old clots are less effective. Of course, thrombolysis is only the first step in the treatment of pulmonary embolism, and the subsequent anticoagulation therapy is the “protracted battle” of the patient’s treatment. For most patients with pulmonary embolism, anticoagulation alone can achieve the therapeutic effect. The duration of subsequent anticoagulation varies for different causes of pulmonary embolism, ranging from 3 months to a lifetime of medication. Let’s first understand the two common anticoagulants, warfarin and low molecular heparin. These two drugs have different usage, different mechanism of action, and different duration of onset and maintenance of effects. The thrombus is attached to the blood vessel wall 2. The thrombus is dislodged and floats with the blood flow Oral anticoagulant “warfarin” is the most common drug used by patients after they go home from the hospital because warfarin is an oral drug and easy to take. How does it inhibit the formation of blood clots? First, let’s understand the ingredients of thrombosis. Coagulation factors are an important factor in the formation of blood clots, and vitamin K is a raw material for the formation of coagulation factors. In the absence of vitamin K, clotting factors cannot be synthesized and blood clots cannot be formed. Warfarin captures this point by inhibiting vitamin K in the body from participating in the synthesis of clotting factors II, VII, IX and X in the liver, thus reducing clotting factors and preventing clot formation. How should I take warfarin? It does not have a fixed dose to take, and each patient takes a different dose. During hospitalization, the doctor will adjust the medication according to the “INR” value of the coagulation function. Since coagulation is usually rechecked in the morning, it is recommended that patients take the medication in the afternoon or evening and at a fixed time each day, so that if there is an adjustment to the dose, it can be changed the same day. Some patients may miss a dose when taking medication. If you miss a dose on the day you think about it, you can just take it at the wrong time and eat it according to the original dose; if you think about it the next day, you should not make up for the previous day’s medication. An occasional missed dose has little effect on coagulation function, but multiple missed doses can result in high and low INR values, which may increase the patient’s risk of bleeding and recurrence of thrombosis. Warfarin is not well suited for patients requiring emergency anticoagulation because of its slow onset of action, which usually takes 5 days after dosing to take effect. When patients switch from low molecular heparin to oral warfarin, the two drugs need to be combined for at least 5 days. Waiting for warfarin to take effect and then stopping the low molecular heparin prevents an increased risk of thrombosis during the switch. However, once warfarin takes effect, the effect will last for almost a week (5-7 days) and is effective for long-term anticoagulation therapy. “Belly shot” low molecular heparin low molecular heparin is a subcutaneous injection, which needs to be injected into the abdomen and other fatty areas. It acts as an anticoagulant by inhibiting the activity of coagulation factor Xa (a clotting substance). Low-molecular heparin works quickly, so it will be injected first to keep the patient’s hypercoagulable state under control before using warfarin for long-term maintenance. Patients with thrombosis are also usually treated with low molecular heparin if they have had recent bleeding. Because the effect of each low-molecular heparin is fixed, while warfarin needs to be adjusted according to the INR value, if the dose of the drug is high, it will aggravate the bleeding risk of the patient. Whether it is warfarin or low molecular heparin, there is no major difference in the anticoagulant effect between the two, and they are generally used alone, with only the overlap required when low molecular heparin is overdosed to warfarin. In general, it is crucial to administer the medication on time and according to the dosage.