Pathogenesis of acute hemorrhage syndrome

Abstract

Circulation blood volume reduction, vascular tone change and decreased cardiac output are the three major factors constituting the acute hemorrhage syndrome pathogenesis that has originally been referred to as “hemorrhagic shock”. Vascular trend with secondary redistribution of the blood volume and following microcirculatory changes as well as the cellular one with principal metabolic modifications are considered to be the leading ones in the development of shock. After the establishment of the leading role of acute hypovolemia and anemia this phenomenon has been labeled “acute posthemorrhagic anemia syndrome”. The development of polyorganic insufficiency syndrome after acute hemorrhage is to a great extent associated with oxygen transport disturbance due to circulatory hypoxia and to a lesser one — with haemic hypoxia due to circulating red blood cells and hemoglobin deficit. Profound tissue metabolism disorders persist even after central hemodynamics and microcirculatory perfusion restoration thus considerably decreasing the nonspecific immune defense and the ability of tissues to reparation and enhancisng proinflammatory and destructive tendencies.