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Siegel GJ, Agranoff BW, Albers RW, et al., editors. Basic Neurochemistry: Molecular, Cellular and Medical Aspects. 6th edition. Philadelphia: Lippincott-Raven; 1999.

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Basic Neurochemistry: Molecular, Cellular and Medical Aspects. 6th edition.

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Hypercapnic Encephalopathy

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Respiratory acidosis leads to decreased brain pH

Patients with chronic pulmonary disorders may exhibit lethargy, confusion, memory loss and stupor. The combined insults of hypoxia and hypercapnia, which result in CO2 retention, contribute to the encephalopathy, but neurological symptoms correlate best with the degree of CO2 retention. Acute moderate hypercapnia, 5 to 10% CO2 in the expired air, leads to arousal and excitability, whereas higher CO2 concentrations, >35% in the expired air, are anesthetic.

Although CO2 is a normal metabolite, it is toxic at elevated levels. CO2 exists in equilibrium with carbonic acid (H2CO3) and with bicarbonate (HCO3), a major H+ buffer. Renal conservation of HCO3 is generally sufficient to buffer hypercapnia; however, an added insult, such as an infection, fatigue or ingestion of a sedative, may further compromise pulmonary function, resulting in further CO2 retention and disruption of the normal buffering mechanisms. The respiratory acidosis associated with CO2 retention in blood leads to a proportional increase in brain tissue [H+].

The combination of hypoxia and hypercapnia in pulmonary insufficiency results in cerebral vasodilation and increased CBF and may lead to increased intracranial pressure. Arteriovenous differences for oxygen across the brain generally decrease as a function of increased CBF, leaving CMRO2 unchanged [28].

Acute hypercapnic acidosis leads to an increase in concentrations of glycolytic intermediates above the phosphofructokinase step, and a decrease below this step is likely due to inhibition of phosphofructokinase by [H+]. Brain ATP concentrations are unchanged in hypercapnia, and it is generally believed that decreased CMRglc is the result of decreased neuronal activity and, hence, reduced fuel, that is, glucose requirements. Neurotransmitter-related mechanisms which could contribute to hypercapnic encephalopathy include decreased neurotransmitter glutamate pools and decreased synthesis of acetylcholine.

By agreement with the publisher, this book is accessible by the search feature, but cannot be browsed.

Copyright © 1999, American Society for Neurochemistry.
Bookshelf ID: NBK28164

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