5.5 Haemostasis
Leanne Dooley
Learning Objectives
By the end of this section, you will be able to:
- Describe the three mechanisms involved in haemostasis
- Explain how the extrinsic and intrinsic coagulation pathways lead to the common pathway and the coagulation factors involved in each
- Discuss disorders affecting haemostasis
Platelets are key players in haemostasis, the process by which the body seals a ruptured blood vessel and prevents further loss of blood. Although rupture of larger vessels usually requires medical intervention, haemostasis is quite effective in dealing with small, simple wounds and small internal bleeds. There are three steps to the process: vascular spasm, the formation of a platelet plug, and coagulation (blood clotting). Failure of any of these steps will result in haemorrhage—excessive bleeding. The vascular response and platelet plug formation are referred to as primary haemostasis and coagulation is referred to a secondary haemostasis.
Vascular Spasm
When a blood vessel is severed or punctured, or when the wall of a vessel is damaged, vascular spasm occurs. In vascular spasm, the smooth muscle in the walls of the vessel contracts dramatically. This smooth muscle has both circular layers; larger vessels also have longitudinal layers. The circular layers tend to constrict, which narrows the vessel lumen, and slows the flow of blood. The longitudinal layers, when present, draw the vessel back into the surrounding tissue, often making it more difficult for a surgeon to locate, clamp, and tie off a severed vessel. The vascular spasm response is believed to be triggered by several chemicals called endothelins that are released by vessel-lining (endothelial) cells and by pain receptors in response to vessel injury. This phenomenon typically lasts for up to 30 minutes, although it can last for hours.
Formation of the Platelet Plug
In the second step, platelets, which normally float free in the plasma, encounter exposed underlying connective tissue and collagenous fibres at the site of blood vessel damage. The platelets bind (adhesion) to the exposed collagen and become activated. Activated platelets are spiked and sticky and bind to other activated platelets (aggregation) and the endothelial lining. Platelet adhesion is assisted by a glycoprotein released from neighbouring endothelial cells called von Willebrand factor, which helps stabilise the growing platelet plug. Platelet aggregation is aided by the plasma protein, fibrinogen, which forms bridges between adjacent platelets at the site of bleed vessel damage. As platelets collect, they simultaneously release chemicals from their granules into the plasma that further contribute to haemostasis. Among the substances released by the platelets are:
- adenosine diphosphate (ADP), which helps additional platelets to adhere to the injury site, reinforcing and expanding the platelet plug
- serotonin, which maintains vasoconstriction
- prostaglandins and phospholipids, which al