The events depicted in Fig. 1 show that the delicate balance of clot formation and its lysis is maintained to achieve three main goals. First, blood is kept in the fluid state for adequate oxygen delivery to the tissues. Second, blood loss is minimised by formation of a clot
whenever there is injury to the vessel. Third, clots are lysed after the injury is repaired and the vessel patency is restored.
It is important to understand that the coagulation cascade can be triggered either by intrinsic or extrinsic stimulus. There is a sequential and an overlapping activation of the proenzymes in the presence of the co-factors and the substrates and with the appropriate pH and the temperature of the milieu. At all stages of this cascade, activated enzyme acts as a negative feedback mechanism and forms the rate limiting step.
Prothrombin is converted into thrombin that, in turn, converts fibrinogen into fibrin monomer. These fibrin strands are very weak and can be easily broken down. They are polymerised in the presence of factor XIII or fibrin stabilising factor, to form a strong framework or the skeleton of the clot. Platelets act as a local messenger of the stimulus of injury. They are activated at the site, releasing their granule contents (ADP, serotinin, histamine) with further propagation of the process and strengthening of the clot. This clot may later be lysed or may get organised with infiltration of fibroblasts, depending on the local need of the circulation.
Table 1. Factors Affecting Haemostasis Preoperative Intraoperative Postoperative
Emergency operations Thrombolised patients Re-do surgery Complex surgery Congenital cyanotic heart surgery Renal failure Hepatic failure Diabetis mellitus Endocarditis/sepsis Old age Bleeding diathesis/vitamin deficiency Collagen diseases e.g. Marfan's disease Drugs: aspirin, heparin, warfarin
Prolonged CPB Frail tissues (poor protoplasm) Deep hypothermic circulatory arrest (DHCA) Calcification Local infection with abscess formation
Hypothermia Acidosis Anaemia Heparin rebound (inadequate protamine) Hypertension Excessive agitation of the patient with muscle contractility Coagulopathy/
The intrinsic coagulation pathway is initiated when blood comes into contact with a foreign surface and the factor XII (Hageman factor) is converted into its active form.8,9 Activated factor XII triggers conversion of prekallikrein to kallikrein in the presence of high molecular weight kininogen (HMWK). This, in turn, acts on many pathways including conversion of HMWK to bradykinin, activation of prorenin to renin, complement activation, and conversion of plas-minogen to plasmin, which in turn further activates complement and lyses the clot.
Factors affecting haemostasis preoperatively, intraoperatively and postoperatively can be found in Table 1.
Was this article helpful?