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Response of the Macrocirculation

  • Chapter
Pathophysiology of Shock, Sepsis, and Organ Failure

Abstract

Shock is the physiologic evidence of cellular demand for energy exceeding mitochondrial capability to generate adenosine triphosphate (ATP) aerobically. With the notable exception of septic shock, most forms of shock result from decreases in systemic O2 transport (ṪO2) produced by loss of circulatory volume and heart or respiratory failure. These conditions alter distribution of cardiac output and blood flow (Q̇) within individual organs. These circulatory alterations are the expression of neural, humoral, and local metabolic mechanisms of vascular control that strive to maintain adequate tissue perfusion in vital organs, such as the heart, brain, adrenal glands, and skeletal muscle. Although our knowledge of blood flow redistribution during shock is incomplete, the determinants of organ blood flow during disease are examined in this chapter.

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Authors and Affiliations

  1. Division of Pulmonary and Critical Care Medicine, University of Texas Health Science Center, Houston, Texas, USA

    G. Gutierrez & S. D. Brown

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  1. G. Gutierrez
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  2. S. D. Brown
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Editors and Affiliations

  1. Ludwig-Boltzmann Institute for Experimental and Clinical Traumatology, Donaueschingenstraße 13, A-1200, Vienna, Austria

    Günther Schlag M. D.  & Heinz Redl Ph. D.  & 

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© 1993 Springer-Verlag Berlin Heidelberg

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Gutierrez, G., Brown, S.D. (1993). Response of the Macrocirculation. In: Schlag, G., Redl, H. (eds) Pathophysiology of Shock, Sepsis, and Organ Failure. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-76736-4_16

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  • DOI: https://doi.org/10.1007/978-3-642-76736-4_16

  • Publisher Name: Springer, Berlin, Heidelberg

  • Print ISBN: 978-3-642-76738-8

  • Online ISBN: 978-3-642-76736-4

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