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The Cerebrovascular CO 2 Reactivity during the Acute Phase of Brain Injury
Author(s) -
Gold Georg E.,
Jensen Finn Taagehøj,
Malmros Richard
Publication year - 1977
Publication title -
acta anaesthesiologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.738
H-Index - 107
eISSN - 1399-6576
pISSN - 0001-5172
DOI - 10.1111/j.1399-6576.1977.tb01213.x
Subject(s) - hypocapnia , medicine , anesthesia , reactivity (psychology) , ventilation (architecture) , perfusion , hyperventilation , cardiology , traumatic brain injury , hypercapnia , acidosis , pathology , mechanical engineering , alternative medicine , psychiatry , engineering
Using the intra‐arterial 133 xenon ( 133 Xe) method, the cerebrovascular response to acute Pa Co2 reduction was studied in 26 unconscious, brain‐injured patients subjected to controlled ventilation. The CO 2 reactivity was calculated as δ In CBF/δ Pa co2 . The perfusion pressure was defined as the difference between mean arterial pressure and mean intraventricular pressure. Although the CO 2 reactivities did not differ significantly from that in awake, normocapnic subjects, it was low in the acute phase of injury, especially in those patients with severe outcome in whom the brain‐stem reflexes were often affected. An increase of the CO 2 reactivity with time was observed, indicating normal response after 1–2 weeks. Chronic hypocapnia in six unconscious patients resulted in sustained CSF pH adaptation. The question whether a delay in CSF pH adaptation exerts an influence on the CO 2 reactivity, and the influence of cerebral lactacidosis on the CO 2 response are discussed.