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Pathophysiology of VO2/DO2 in Sepsis

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Applied Cardiovascular Physiology

Part of the book series: Update in Intensive Care and Emergency Medicine ((UICM,volume 28))

Abstract

The high molar demand for oxygen (02) compared to other metabolic substrates implies that tissues deplete blood of 02 much sooner than of these other substrates. Under normal resting conditions, tissue 02 demand rather than tissue 02 supply (DO2) determines the rate of 02 uptake (VO2). When blood carries less than the normal amount of 02 or when blood flow is reduced, DO2 is reduced and compensatory adjustments occur in an attempt to satisfy the 02 requirements of peripheral tissues. As DO2 is gradually reduced, 02 consumption (VO2) is maintained by increases in the 02 extraction ratio (ER02 = VO2/DO2), until a critical point at which VO2 falls with further declines in DO2. At this critical point, tissues shift toward a chemically reduced state with elaboration of reduced substrate forms such as lactate. It has been proposed that increased ER02 is a consequence of regulation of the circulation and the result of the simultaneous activation of both central and local factors. Central factor induces a regional redistribution of blood flow among tissues via sympathetic vasoconstrictor tone while local factor or autoregulation induces an increase in the density of perfused capillaries within tissues via metabolic vasodilator tone. Local autoregulatory processes include local release and action of vasodilating substances. An inability to regulate blood flow distribution, between and within tissues, could result in hyperperfusion of some tissue beds at the expense of other hypoperfused areas resulting in 02 extraction defect as seen in sepsis.

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Authors
  1. B. Vallet
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Editors and Affiliations

  1. Dept. of Anesthesiology and Critical Care Medicine, University of Pittsburgh, 604 Scaife Hall, Pittsburgh, PA, 15261, USA

    Michael R. Pinsky

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© 1997 Springer-Verlag Berlin Heidelberg

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Vallet, B. (1997). Pathophysiology of VO2/DO2 in Sepsis. In: Pinsky, M.R. (eds) Applied Cardiovascular Physiology. Update in Intensive Care and Emergency Medicine, vol 28. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-60696-0_17

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  • DOI: https://doi.org/10.1007/978-3-642-60696-0_17

  • Publisher Name: Springer, Berlin, Heidelberg

  • Print ISBN: 978-3-642-64512-9

  • Online ISBN: 978-3-642-60696-0

  • eBook Packages: Springer Book Archive

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