The ability to control bleeding hinges primarily on the availability and adequate functionality of platelets and coagulation factors. However, it is essential to note that there are limits to the size or degree of damage that can be controlled and repaired without outside (medical) intervention. As one may expect, and the diagram illustrates, damage to a larger vessel yields a more substantial bleed and, in turn, consumes a greater quantity of coagulation components. These variables can radically alter the effectiveness of hemostatic control mechanisms.
As we will discover later in the course, other variables impact the effectiveness of hemostatic mechanisms, such as acquired disease states and inborn metabolic pathway defects. For now, however, our focus will be on the mechanisms, processes, and components that work together to achieve coagulation or the cessation of blood flow from a damaged vessel.
Note: Although the word hemostasis refers to the coagulation mechanism and the function and interaction with the vascular and extravascular systems and platelets, the terms hemostasis and coagulation are commonly used interchangeably, as this course demonstrates.
