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30 - Acidosis/alkalosis

from Part IV - Specific Conditions Associated with Fetal and Neonatal Brain Injury

Published online by Cambridge University Press:  10 November 2010

Robert C. Vannucci
Affiliation:
Pennsylvania State University College of Medicine, Hershey, PA, USA
David K. Stevenson
Affiliation:
Stanford University School of Medicine, California
William E. Benitz
Affiliation:
Stanford University School of Medicine, California
Philip Sunshine
Affiliation:
Stanford University School of Medicine, California
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Summary

Introduction

The pH regulation of the blood is a critical physiologic process necessary to maintain optimum metabolism of body tissues, including the brain. Accordingly, the maintenance of a normal blood pH is of paramount importance for physicians to prevent the untoward effects of acidosis or alkalosis. Respiratory acidosis and alkalosis, as well as metabolic acidosis, are frequently encountered in sick premature and full-term newborn infants. Respiratory acidosis occurs as a consequence of respiratory distress syndrome and other pulmonary disease, while respiratory alkalosis typically occurs as an iatrogenic component of the hyperventilation necessary to oxygenate adequately a critically ill newborn infant. Metabolic acidosis with or without respiratory acidosis typically arises from systemic hypoxia or asphyxia in the fetus or newborn infant. The present chapter will review available information regarding pH regulation of cerebral blood flow (CBF) and metabolism under physiologic conditions and the contribution of acidosis/alkalosis to brain damage, especially that arising from cerebral hypoxia–ischemia.

Effect of respiratory acidosis/alkalosis on cerebral blood flow

Cerebral blood vessels are known to be sensitive to changes in Paco2, such that CBF is increased during respiratory acidosis and decreased during respiratory alkalosis. These CBF responses to changes in Paco2 exist in the fetus and newborn animal, including the newborn infant, although the sensitivity of immature cerebral blood vessels is not as well developed as in the adult. Investigations have been conducted in a variety of animal species, including dogs, pigs, sheep, and monkeys.

Type
Chapter
Information
Fetal and Neonatal Brain Injury
Mechanisms, Management and the Risks of Practice
, pp. 593 - 611
Publisher: Cambridge University Press
Print publication year: 2003

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  • Acidosis/alkalosis
  • Edited by David K. Stevenson, Stanford University School of Medicine, California, William E. Benitz, Stanford University School of Medicine, California, Philip Sunshine, Stanford University School of Medicine, California
  • Book: Fetal and Neonatal Brain Injury
  • Online publication: 10 November 2010
  • Chapter DOI: https://doi.org/10.1017/CBO9780511544774.032
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  • Acidosis/alkalosis
  • Edited by David K. Stevenson, Stanford University School of Medicine, California, William E. Benitz, Stanford University School of Medicine, California, Philip Sunshine, Stanford University School of Medicine, California
  • Book: Fetal and Neonatal Brain Injury
  • Online publication: 10 November 2010
  • Chapter DOI: https://doi.org/10.1017/CBO9780511544774.032
Available formats
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To save content items to your account, please confirm that you agree to abide by our usage policies. If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account. Find out more about saving content to Google Drive.

  • Acidosis/alkalosis
  • Edited by David K. Stevenson, Stanford University School of Medicine, California, William E. Benitz, Stanford University School of Medicine, California, Philip Sunshine, Stanford University School of Medicine, California
  • Book: Fetal and Neonatal Brain Injury
  • Online publication: 10 November 2010
  • Chapter DOI: https://doi.org/10.1017/CBO9780511544774.032
Available formats
×