Clinicai and therapeutic aspects of the state of shock

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;


Irineu Tadeu Velasco*
Clinicai and therapeutic aspects of the state of shock S hock 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; • modulates the excessive release of vasopressin and; • indicates (suggests) a lnodulation of the inflammatory response In volun1etric replacelnent with whatever expander, we lnust associate vasoactive drugs if an average PA of > 60 lnHg is not maintained.The next step is to lllonitor the patient and try to achieve a cardiac rate above 2.2 in cardiogenic shock, and above 4.0 -4.5 in sepsis and hypovolemia.
As to the mediators involved, in sepsis a bacterial endotoxin can provoke an increase in TNF and interleucinas 1,6 and 8, which in turn release nitric oxide and cause arterial vasodilation.The use of Illonoclonal antibodies against endotoxin or taurolidin does not lower lllortality in sepsis.On the other hand, the use of the anti-TNF antibody increases survival in sepsis.
The use of n-metil arginin, which reduces the release of nitric oxide, still requires Inore conclusive tests as to its benefits in sepsis.The inhalatory use of nitric oxide shows an improvement in the ratio perfusion-ventilation.
In the control of a patient in shock, it is ilnportant to Illonitor the regional flow distribution and eventual organic failures (renal and hepatic insufficiencies, Illental confusion and CIUD).The lactate and the intralllucosal pH, and the enZYllles and proteins of the affected organs could be useful in following the patient.
SOlne procedures.incardiac shock in acute lllyocardial infarction deserve consideration, such as angioplastia anel revascularization through medication or surgery.
In conclusion, it IllUSt be stressed that despite the sophistication of the propedeutics, new Illedi'cations anel lllechanisms in the treatment of shock, nothing.substitutes the physician being constantly at the patient's side, knowing how to interpret the significance of sYlnptollls (mental confusion, paleness, sweatiness, tachycardia, cyanosis, base stertor, PVC, etc.) for the success of the therapy.

*
Full professor of lhe Emergency Medicine Discipline, Faculty of Medicine -University of São Paulo.VELASCO, !.T. -Clinicai and therapeutic aspects of the state of shock