2 resultados para Sociedad Médica General de Socorros Mutuos.

em BORIS: Bern Open Repository and Information System - Berna - Suiça


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Myocardial dysfunction appears in 25% of patients with severe sepsis and in 50% of patients with septic shock, even in the presence of hyper dynamic states. It is characterized by a reduction in left ventricle ejection fraction, that reverts at the seventh to tenth day of evolution. Right ventricular dysfunction and diastolic left ventricular dysfunction can also appear. There is no consensus if an increase in end diastolic volume is part of the syndrome. High troponin or brain natriuretic peptide levels are associated with myocardial dysfunction and a higher mortality. The pathogenesis of myocardial dysfunction is related to micro and macro circulatory changes, inflammatory response, oxidative stress, intracellular calcium management disturbances, metabolic changes, autonomic dysfunction, activation of apoptosis, mitochondrial abnormalities and a derangement in catecholaminergic stimulation. Since there is no specific treatment for myocardial dysfunction, its management requires an adequate multi systemic support to maintain perfusion pressures and systemic flows sufficient for the regional and global demands.

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Maintaining an adequate tissue oxygen delivery (DO(2)) and consumption (VO(2)) is crucial in the treatment of septic patients. A fall in V0(2) is associated with a higher mortality. The early recognition of shock or tissue hypo perfusion impacts on patient prognosis. In occasions, hypovolemia or important regional oxygen debts are not recognized, since macro homodynamic variables have been compensated. In this situation, the use of metabolic hypo perfusion markers such as lactate, central venous oxygen saturation and gastric goniometry, can be helpful. However, interpretation of these markers should be cautious and always considering the overall clinical status of the patient. In the initial stages of sepsis, the dependency of V0(2) on DO(2) predominates as histopathological mechanism of multiple organic failure. In late stages, other factors predominate as determinants of multiple organic failure and mortality, such as hyper or hypo immune response, microcirculatory alterations and cytopathic hypoxia.