Activation of Blood Coagulation After Cardiac Arrest Is Not Balanced Adequately by Activation of Endogenous Fibrinolysis

Abstract

Our data clearly demonstrate that there is a marked activation of blood coagulation and fibrin formation after prolonged cardiac arrest and CPR in humans that is not balanced adequately by concomitant activation of endogenous fibrinolysis. These changes may contribute to reperfusion disorders, such as the cerebral "no-reflow" phenomenon, by inducing fibrin deposition and formation of microthrombi.

Time course of circulatory and metabolic recovery of cat brain after cardiac arrest assessed by perfusion- and diffusion-weighted imaging and MR-spectroscopy

“…However, the lack of amelioration of cerebral hypoperfusion with either osmotic or fibrinolytic therapy was not surprising since the pathophysiology of cerebral no-reflow and delayed hypoperfusion differs fundamentally [41]. The pathophysiology of no-reflow is multifactorial and includes vascular factors like obstruction of the capillary lumen by endothelial flaps [42] or compression by swollen perivascular glial cells [43], blood factors like viscosity changes [44], sludging of erythrocytes [45], the formation of platelet aggregates [46] or an imbalance of blood coagulation [47], and general cardiovascular factors like post-ischaemic hypotension [48]. In contrast, the protracted hypoperfusion after global cerebral ischaemia is a functional disturbance due to an increased vasotonus [41].…”

Therapeutic Hypothermia for Cardiac Arrest

“…[32,33] Therapeutic Hypothermia could be beneficial in this instance since platelets number and function are decreased with temperatures <35°C, and some inhibition of the coagulation cascade develops at temperatures <33°C. [34,35] Vasoconstriction , mediated mainly by thromboxane and endothelin plays a pivotal role in the secondary injury as well.…”

Prehospital Therapeutic Hypothermia for Cardiac Arrest

“…[39][40][41] The coagulation cascade is also activated with ischemia-reperfusion injury leading to intravascular clot formation resulting in microvascular thrombosis in the brain. [42,43] Therapeutic Hypothermia could be beneficial in this instance since platelets number and function are decreased with temperatures <35°C, and some inhibition of the coagulation cascade develops at temperatures <33°C. [44,45] Vasoconstriction, mediated mainly by thromboxane and endothelin plays a pivotal role in the secondary injury as well.…”