anticoagulation
Anticoagulation is treatment that slows the blood's ability to clot, the cornerstone of preventing and treating venous thromboembolism. The popular name blood thinning is a little misleading, the blood does not actually become thinner; rather, the chemical chain reaction that builds a clot is dampened, so existing clots stop growing and new ones are less likely to form while the body's own systems dissolve what is already there.
In pulmonary embolism and deep vein thrombosis, anticoagulation does not usually dissolve the clot directly. Its job is to hold the line, preventing extension and new emboli, while the body gradually breaks the clot down over weeks. Several drug families are used, including injectable heparins, the older tablet warfarin which needs blood monitoring, and the newer direct oral anticoagulants that need less monitoring.
The unavoidable trade-off is bleeding. By reducing clotting everywhere, anticoagulation makes harmful bleeding easier too, so every decision balances the risk of a dangerous clot against the risk of a dangerous bleed. The choice of drug, dose, and how long to continue depends on what provoked the clot, the chance of recurrence, and individual bleeding risk.
Anticoagulation prevents and contains clots; it does not actively dissolve them. Drugs that actively break clots apart are called thrombolytics and are reserved for the most severe cases because they carry a much higher bleeding risk.