Haemostasis
This section describes the role of haemostasis and the importance of balancing its constituent processes in healthy vascular function
In this section:
Haemostasis is essential for survival
- Haemostasis is the normal physiological response that prevents significant blood loss after vascular injury1
- Haemostasis depends on an intricate series of events involving platelets, other blood cells, such as TF-bearing cells, and the activation of specific blood proteins, known as coagulation factors1
- Knowledge of haemostasis is important in understanding major disease states associated with thrombosis, such as:
- VTE
- Atherothrombosis (thrombosis triggered by plaque rupture)
- Cardioembolic stroke
- Knowledge of haemostasis is important in understanding major disease states associated with thrombosis, such as:
Initiation of haemostasis
- When blood vessel injury occurs, physiological haemostasis is triggered and the sequence of events listed below takes place:
- The vessel constricts to reduce blood flow
- Circulating platelets adhere to the vessel wall at the site of trauma
- Platelets are activated and aggregate
- An intricate series of enzymatic reactions occur involving coagulation proteins
- Fibrin is produced to form a stable haemostatic plug
Balancing haemostasis
The process of coagulation depends on a complex interplay of enzymatic and cellular activity, culminating in the formation of a stable vascular ‘plug’. The subsequent process of clot dissolution that occurs during the healing phase is known as fibrinolysis
References
- Colman RW, Clowes AW, George JN et al. Overview of hemostasis. In: Colman RW, Clowes AW, George JN et al (eds). Hemostasis and thrombosis: basic principles and clinical practice. 5th edn. Philadelphia: Lippincott, Williams & Wilkins; 2006. p. 1–16. Return to content
- Adams GL, Manson RJ, Turner I et al. The balance of thrombosis and hemorrhage in surgery. Hematol Oncol Clin North Am 2007;21:13–24. Return to content
- Heit JA. Venous thromboembolism: disease burden, outcomes and risk factors. J Thromb Haemost 2005;3:1611–1617. Return to content