Blood is contained within the cardiovascular system – the heart and blood vessels – with additional amounts stored in the liver and spleen. The quantity of blood in the human body is approximately 5.5 liters. When bleeding, up to 20% of this total blood volume can be lost without a person being at risk provided that the necessary reflexes take effect. However, this cannot continue unabated and the body has a number of interrelated mechanisms to prevent excessive or prolonged blood loss.
What is hemostasis?
Hemostasis is the body’s series of processes developed to prevent blood loss when a vessel is compromised. It literally means to ‘stop blood’ and if the hemostatic mechanisms are working as it should it will be able to achieve this goal. Simply, hemostasis is the blood clotting process but a number of mechanisms exist before and after the formation of the actual blood clot. Without hemostasis, bleeding would continue unabated and eventually result in death. This process although efficient does have its limitations with severe hemorrhages.
Steps in Hemostasis
There are broadly four steps in the process of hemostasis.
- Vascular phase – vascular constriction
- Platelet phase – formation of a platelet plug
- Coagulation phase – blood clot formation
- Fibrosis and fibrinolysis – fibrous tissue growth or clot dissolution
The first step takes effect almost immediately after there has been a break in the blood vessel and may even occur with injury to the blood vessel without a tear. The tear is sealed anywhere within a few minutes to about 20 minutes. The final process that permanently seals the blood vessel may only be completed about 1 to 2 weeks after the initial injury.
Constriction of the blood vessel that is torn starts almost immediately after the injury. Since blood vessels have smooth muscle in it wall, reflexes narrow the lumen of the blood vessel thereby drastically reducing blood flow through the vessel. This also means that minimal blood is loss compared to the blood loss that would have occurred without these reflexes. Vasoconstriction in this manner occurs through three processes.
- Firstly the injury causes the local myogenic reflexes to take effect thereby causing vascular spasm.
- Then the chemicals, like thromoxane A2, released by vessel wall injury and platelets further contributes to the constriction. These are known as local autacoid factors.
- Lastly sensory impulses, possibly pain, stimulate nerve reflexes to promote vasoconstriction.
The degree of vasoconstriction appears to be related to the degree of injury. Therefore a severely ruptured blood vessel will constrict more intensely than a minor cut of the vessel wall. Vasoconstriction may last for up to hours until the other blood clotting processes take effect to restore the integrity of the compromised blood vessel.
Platelet aggregation and activation forms a plug before the blood clot. Platelets are tiny disc-shaped components of blood that are in constant circulation. It is formed by the fragmentation of large megakaryocytes and are constantly sealing tiny holes in the blood vessels that occur everyday even without trauma. Despite being a cell fragment and lacking the ability to divide, platelets are essentially functioning units. It contains important enzymes and chemical factors to complete its action and has mitochondria for energy supply. These enzymes and chemical factors have a diverse number of functions including promoting blood clotting and repairing the wall of the blood vessel.
Under normal circumstances, platelets will not attach to the inner lining of the blood vessel (endothelium). The cell membrane of platelets has specialized glycoproteins that repel it from the endothelium. However, the moment the blood vessel wall is compromised, the platelets are strongly attracted to the site of injury. Once attached, the platelet swells and portions of it extend outwards to attached to neighboring platelets or other portions of the torn vessel wall. The platelets can also contract to form a tight and firm plug. The platelets also become sticky by the action of certain clotting components like thromboxane A2 and von Willebrand factor. This stickiness ensures that more platelets firmly attach to the already activated platelets.
The formation of a blood clot provides a more long lasting plug. The clotting process involves the laying down of fibrin which reinforces the platelet plug. Fibrin is a long protein strand which forms from fibrinogen by the action of thrombin. The fibrin then forms a mesh network in which some blood cells and fluid also get trapped along with the platelets.
Once the clot is tightly secured to all the torn parts of the vessel wall, it retracts and pulls the edges of the broken vessel wall closer. This retraction is sometimes discussed as a separate phase of hemostasis. The retraction firmly seals the tear in the vessel wall. The entire process is mediated by a range of chemicals known as procoagulants which are circulating in the blood. Some of the clotting factors also referred to as the coagulation factors includes Factor I to Factor XIII (factors 1 to 13) although the Factor VI (factor 6) does not exist, prekallikrein and kininogen. The process of coagulation is complex and involves different pathways to achieve the desired effect.
Fibrosis and Fibrinolysis
Once a clot forms, the blood vessel wall will slowly heal. The clot may either dissolve or form a patch of fibrous tissue (scar). The latter is usually only seen with a severely damaged blood vessel where fibroblasts enter the clot and causes organization. Usually enzymes will dissolve the blood clot in a process known as fibrinolysis once the vessel wall is suitably repaired.