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Shock is seen as a sequence of events initiated by an aggressive factor (hypovolumetric traulna, burns, sepsis) followed by a endocrine response (release of ACTH, adrenaline, vasopressin) and a failure in the maintenance lnechanism of homeostasis at the hemodynalnic leveI, with a decrease in effective tissue perfusion. This leads to cellular ischemia and to the release of cytokinins (a factor in tumoral interleucinas necrosis 1,6 and 8, nitric oxide and endothelins) which result in a systemic inflamlnatory process, which, if not controlled in tiIne, becolnes irreversible. The treatment itself can accentuate the inflammatory process, which is called, reperfusion lesion. The diagnostic is clinicaI, instrumental and laboratorial, and the objectives of treatment are: • to prevent the aggressiv~ factors (a public heath lneasure); • to replace the lost volume in accordance with the type of aggression; • to monitor the endocrinal response, and before the fact to try to modulate the release of catecholamines and vasopressin; • to the Ílnprove the effective tissue perfusion; • to modulate the release of cytokinins and; • to lnininlize the inflammatory process and reperfusion lesions. In the replacement of voJulne, a hypertonic solution of sodium chloride (NaCL) 7.5% has been shown to have great potential because it: • is low cost and rapidly portable to the aggression site; • causes rapid hemodynamic improvement; • improves all-over tissue edema; • improves tissue perfusion through volumic expansion and a decrease in the endotelio edelna of microcirculation;

Clinical and therapeutic aspects of the state of shock