[Pathogenic role of intracellular energy insufficiency (hypoenergy) in the development of circulatory collapse (hemodynamic shock)].

Hemodynamic shock syndrome represents an acute circulatory failure due to a decrease of arteriovenous pressure gradient. Three unrelated groups of processes, cardiogenic, vasohypotonic and hypovolemic mechanisms, are possible starting points of the shock syndrome pathogenesis. The basic features of those principal pathogenic steps are outlined in the paper. In addition, clinical practice very often encounters a complex forms of the syndrome, which include two or all three basic pathogenic mechanisms simultaneously. Direct consequence of arteriovenous pressure gradient loss is diminishing perfusion of tissues. Tissue hypoperfusion causes a progressive depletion of cellular energy rich compounds. Such lowering of cellular ATP concentration (cellular hypoenergosis), very often less than 0.1 mmol/L, plays an important pathogenic role in the conversion of homeostatic regulation processes from a negative into a positive feedback mode. Positive feedback regulation amplifies deterioration of arteriovenous blood pressure gradient loss, which reversely intensifies the degree of energy depletion in tissues. Individual cell death decreases a tissue adjustment capacity to hypoperfusion. The critical step leading to a decompensation (systemic failure) or progressive phase of the shock is the reversal of the homeostasis into the positive feedback mode of action. Final outcome of the syndrome reflects a degree of compensation capacity loss as well as irreversible tissue alterations. Clinical manifestations correlate with the underlying pathogenic processes. Short summary of clinical correlative relations with the pathogenic processes, at the cellular, molecular and/or energy level, is given in the paper.