8.2.1 Haemostasis and evolution

A brief reminder of the physiological phenomena of coagulation is useful for understanding anticoagulation, mandatory for all extracorporeal circuits, and for the management of patients suffering from coagulopathies, whether in cardiac or non-cardiac surgery, in intensive care or in the emergency department.

Coagulation in animal evolution

The most developed invertebrates already have a basic system for haemostasis. In crabs, for example, a vascular lesion causes the aggregation of circulating haemocytes and the formation of a protein gel (coagulin) obtained by cleavage of a circulating protein (coagulogen) under the effect of a serum protease (coagulase located in the granules of the haemocytes) [3]. This is a simplified but identical scheme to that of the coagulation cascade known in mammals. It is necessary because blood has become the main oxygen carrier (which is not the case in insects, for example) and because arterial pressure is higher (40-60 mmHg) in upper invertebrates (crabs, octopuses); it is therefore imperative to quickly seal gaps in the vascular tree.

Chordates are vertebrates ancestors (see Appendix C, page 3), which are currently represented by primitive fish from which lampreys originated 450 millions years ago. These animals already had a coagulation cascade practically identical to that of mammals. This system was therefore set up at the bifurcation between invertebrates and vertebrates, dating back 550 to 450 million years ago. It consists of a chain of successive factors that circulate in plasma in an inactivated and soluble state, but which can give rise to fibrin when an endothelial rupture leads to aggregation of platelets at lesion level. This reaction must remain localised to the pathological area to ensure impermeability, which is imperative because of the high arterial pressure (60-150 mmHg), but it must not spread throughout the vascular tree. A number of elements prevent  blood from clotting unexpectedly [1].

  • A laminar blood flow.
  • An intact endothelium.
  • A relative excess of antiplatelet and anticoagulant substances secreted by the endothelium; almost every stage of coagulation has a plasma inhibitor.
  • Circulating coagulation factors in an inactive and soluble state.
  • The need for a local stimulus to trigger coagulation.
  • The development of the coagulation cascade only on suitable cell surfaces (platelets).
  • The presence of serum proteases able to degrade activated factors  escaped into the general circulation.

This whole complex system works on a dynamic balance between procoagulant and anticoagulant agents.

 

© CHASSOT PG, MARCUCCI Carlo, last update November 2019.

 

References

1. ADAMS RLC, BIRD RJ. Review article: Coagulation cascade and therapeutic update: Relevance to nephrology. Part I:       Overview of coagulation, thrombophilia and history of anticoagulants. Nephrol 2009; 14:462-70

3.  AIRD WC. Hemostasis and irreducible complexity. J Thrombosis Haemost 2003; 1:227-30