Abstract
The changes of hemodynamic and oxygen transport variables in human septic shock are well documented [1]. They are essentially characterized by a hyperdynamic circulatory state associated with an increased cardiac output (CO), a decreased systemic vascular resistance (SVR) and a narrowed arterial-mixed venous oxygen difference (a-vO2) together with elevated arterial blood lactate levels. Therefore, when arterial oxygenation is maintained, oxygen delivery (DO2) is as a consequence usually supranormal. This implies a defective tissue oxygen extraction as the most important mechanism that limits oxygen consumption (\( \dot{V}{{O}_{2}} \)) in septic shock. Throughout a septic episode the basic pathophysiologic problem seems to be a disparity between the uptake of oxygen and the demand of oxygen in the tissues as manifested by increased blood lactate levels. Limitation of oxygen uptake may significantly contribute to morbidity and mortality by predisposing to multiple organ failure. Several observations suggest that inadequate tissue oxygenation is a central mechanism mediating the widespread and irreversible tissue damage that is associated with multiple organ failure and a fatal outcome [2, 3].
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Thijs, L.G., Groeneveld, A.B.J. (1991). Tissue Oxygen Utilization in Septic Shock. In: Gutierrez, G., Vincent, J.L. (eds) Tissue Oxygen Utilization. Update in Intensive Care and Emergency Medicine, vol 12. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-84169-9_16
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DOI: https://doi.org/10.1007/978-3-642-84169-9_16
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