Hemostasis: The Prevention Of Blood Loss

Blood flow continually through out blood vessels under the influence of controlled and effective mechanism however, in case of any damage to the blood vessel wall, a cascade of reaction is initiated to stop the bleeding, called hemostasis.

The hemostasis can be defined as a physiological process which leads to the cessation of bleeding at the injury spot and sustains the normal blood flow in the circulation. without this remarkable protection system.

We would rapidly seep out our entire blood volume from even the most minor cuts; a condition called hemorrhage.

Hemostasis is best in managing injuries in small vessels-arterioles, capillaries, venules; which are the most widely perceived bleeding sources in everyday existence. there are two main phases of the hemostasis; primary hemostasis refers to the platelet aggregation and platelet plug formation while secondary hemostasis refers to the deposition of insoluble fibrin, which is generated by the coagulation cascade. this insoluble fibrin forms a mesh that is consolidated into and around the platelet Pluto reinforce and stabilize the blood clot. these two processes happen simultaneously and are mechanistically interwoven.

During hemostasis, following three interlinked steps occur in rapid sequence.

Vascular Spasms or vasoconstriction

The endothelial cells of the intact blood vessels have natural anticoagulant mechanism. they express a fibrinolytic heparin molecules and a receptor, thrombomodulin, which prevents platelets aggregation and stops the coagulation cascade. when a blood vessel is severed of or injured; a prompt, transient and inherent response occurs during which the smooth muscles present in the blood vessels wall contract. it causes constriction of the vessels resulting in the slow progression of blood flow in the affected area. the vasoconstriction response is set off by factors such as a direct injury to the vascular smooth muscle; nervous system reflexes initiated by local pain receptors and signaling molecules released by injured endothelial cells and activated platelets (such as thromboxane A2 and serotonin). A firmly constricted artery can diminish blood loss for 20-30 minutes, lessening the damage and setting up the vessel for the later steps of hemostasis.

Platelet plug formation

The second critical step in hemostasis, which follows vasoconstriction, is formation of platelet plug also known as a hemostasis plug or platelet thrombus. platelets play a vital role in forming this plug by briefly sealing the break in the vessel wall. the three steps of platelet plug formation are platelet adherence, activation, and aggregation.

platelet Adherence

Injury to the blood vessels disrupts the endothelium and collagen from the extracellular matrix beneath the endothelial cells is exposed. the endothelial cells and platelets release a plasma protein called von Waller and factor. (vWF),which is responsible for the adherence of platelets to the collagen by changing their conformation. the vwf binds to the exposed collagen and holds fast the platelet at the injury spot, thus bridging the gap between platelets and damaged vessels.

Additionally, the platelets become sticky and adhere distinctly to the uncovered collagen molecules.

Platelet Activation

Once the platelets get adherent to collagen they are activated to release various cytokines and chemical mediators through degranulation. the release chemical include Adenosine diphosphate (ADP), vWF, thromboxane A2, platelet- derived growth factor (PDGF),vascular endothelial growth factor (VEGF), serotonin and coagulation factors.

Platelet Aggregation

The final step of platelet plug formation is the aggregation of the platelets into a barrier-like plug Receptors on the platelet bind vWF and fibrinogen molecules. which hold the platelet together. the ampleness of the platelet plug is upgraded by the contraction property of platelets ,due to the high concentration of actin and myosin. the completed plug covers the damaged components of the endothelium and prevents blood from flowing out.

If the wound is minor , the platelet plug may be sufficient to stop the bleeding without the coagulation cascade. however, if the wound is adequately large, blood would not coagulation until the fibrin is produced through the  coagulation cascade, reinforcing the platelet plug.