Abstract
Sepsis is the systemic inflanimatory response of the body to the serious infection that occurs once pathogens invade the bloodstream. It remains a leading cause of morbidity and mortality in hospitalized patients, especially those in ICU. Many of the overt physiologic and metabolic components of the systemic response to sepsis are fully characterized. The hypermetabolism which develops early in the course of the disease and which is associated with increased catabolism of the lean body mass (principally skeletal muscle) is well described. In addition, septic patients typically are febrile and may have defective oxygen utilization and elevated circulating lactate levels [1,2]. Ongoing sepsis, in the absence of successful therapeutic Intervention, is characterized by progressive failure of energy metabolism which ultimately causes shock, and death [3]. The pathophysiological Syndrome of shock constitutes a failure of the circulation to meet the metabolic requirements of the tissues. The neurohumoral response to volume loss or inadequate perfusion serves to redistribute flow such that the function of the heart is preserved at the expense of skin, kidney, splanchnic and skeletal muscle perfusion. Although shock is often de– fined, and manifest, in hemodynamic terms as hypotension and inadequate tissue perfusion, the essential defect may ultimately be one of cellular metabolic dysfunction.
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Jacobs, D.O., Mann, D.V. (1993). Changes in Skeletal Muscle Energetics During Sepsis. In: Vincent, JL. (eds) Yearbook of Intensive Care and Emergency Medicine 1993. Yearbook of Intensive Care and Emergency Medicine 1993, vol 1993. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-84904-6_3
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DOI: https://doi.org/10.1007/978-3-642-84904-6_3
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