Why do I have coagulation.
The normal hemostatic (clotting) process, i.e., coagulation, has three different phases:
- Injury to the inner (endothelial) lining of a blood vessel
- Initiation of the clotting process via complex biochemical reactions–the clotting cascade
- Clotting cessation and anti-thrombosis with removal of the clot
The ability to clot is the part of healing (hemostasis) that stops bleeding, but when the clotting process is exaggerated, thrombi (clots) can form within blood vessels. This not only interferes with the smooth flow of blood, but also risks thrombus fragmentation which can release thrombi (emboli) into the circulation.
In the venous system, these migrating clots will enter the right heart after which they’ll be sent into the pulmonary artery, threatening both lungs and life; in arteries, they can lodge downline and tissue beyond the obstruction will be deprived of oxygenated arterial blood, risking tissue ischemia, infarction, and organ death.
Thrombosis can occur in either veins or arteries, but the more susceptible are the veins, since they are a low-pressure conduit of blood flow.
- Veins: thrombosis creates a physical obstruction and if large enough will either partially or completely obstruct venous blood flow, leading to venous stasis, which alters the flow even more. Venous stasis can lead to venous ulcers and when the clots get infected, thrombophlebitis (inflamed, infected veins).
Thrombophlebitis is very painful and can affect walking, but its biggest risk is if a thrombus breaks off and travels as an embolus to the right atrium of the heart, then by way of the right ventricle to the pulmonary artery. This results in lung impairment distal to it as well as a back up of pressure in the right ventricle. This scenario, pulmonary embolus, is life-threatening.
- Arteries: in the arteries, thrombosis is associated with atherosclerosis–plaque formation which results from hypertension, smoking, obesity, dyslipidemia (abnormal cholesterol and triglyceride levels), as well as an inherited genetic predisposition. Obstruction threatens the oxygenated arterial blood flow to organs beyond the site of blockage, risking tissue and organ death. Examples include the the mesenteric artery, the carotid arteries, or the coronary arteries, resulting in tissue death of the intestines, stroke, or myocardial infarction, respectively. Such risks emphasize the importance of anticoagulation when a person has thromboembolic disease.
Any medication that interferes with the coagulation process is a double-edged sword. Anticoagulation is a balancing act between not enough anticoagulation (ineffective prevention of embolic disease) and too much anticoagulation (risk of hemorrhage). Depending on the patient’s site of thrombosis, different anticoagulants can be chosen, oral vs. parenteral (injections), short-acting vs. long-acting, and other considerations such as physician preference, expense, or patients’ tolerances.