[The pathophysiology of hemodynamic shock syndrome (part one)]

Hemodynamic shock syndrome represents an acute circulatory failure leading to a multiple organ failure. Such circulatory failure develops due to a decrease of arteriovenous blood pressure gradient as a consequence of three independent groups of pathogenic mechanisms (cardiogenic, vasohypotonic and hypovolemic), all of which lead to the common pathogenic pathways. A decrease of arteriovenous pressure gradient induces vasomotoric responses, reactive body fluids redistribution, endocrine, metabolic as well as tissue energy adjustments. In this review a comprehensive synopsis of pathogenic processes is outlined. The cardiogenic mechanisms include the acute systolic and/or diastolic heart failure. Vasohypotonic mechanisms (neurogenic, septic and anaphylactic) are due to vascular tonus missadjustment. Hypovolemia caused by blood, plasma, water and electrolytes losses and/or sequestration, leads to decrease of pressure gradient as soon as the extent of hypovolemia overcomes the compensatory vascular capacity. The decrease of tissue perfusion is direct consequence of the arteriovenous pressure gradient loss. Tissue hypoperfusion causes a progressive depletion of cellular ATP concentration (cellular hypoenergosis), which very often falls lower than 0,1 mmol/L. Cellular hypoenergosis plays the critical role in conversion of negative homeostatic regulation into a positive feedback mode. Positive homeostatic regulation (circuli vitiosi) amplifies deterioration of arteriovenous blood pressure gradient, which reversely intensifies the degree of energy depletion in the tissues. Such homeostatic conversion plays a critical role in the development of progressive phase (systemic failure, decompensation) of the shock.