Noninvasive Estimation of Cerebral Perfusion Pressure and Zero Flow Pressure in Healthy Volunteers: The Effects of Changes in End-Tidal Carbon Dioxide
Zero flow pressure (ZFP) in the cerebral circulation is defined as the arterial pressure at which flow ceases. Noninvasive methods of estimating cerebral perfusion pressure (CPP) and ZFP using transcranial Doppler ultrasonography have been described. There is a paucity of normal physiological data r...
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Published in | Anesthesia and analgesia Vol. 96; no. 3; pp. 847 - 851 |
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Main Authors | , , |
Format | Journal Article |
Language | English |
Published |
Hagerstown, MD
International Anesthesia Research Society
01.03.2003
Lippincott |
Subjects | |
Online Access | Get full text |
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Summary: | Zero flow pressure (ZFP) in the cerebral circulation is defined as the arterial pressure at which flow ceases. Noninvasive methods of estimating cerebral perfusion pressure (CPP) and ZFP using transcranial Doppler ultrasonography have been described. There is a paucity of normal physiological data related to changes in estimated CPP (eCPP) and ZFP induced by changes in carbon dioxide (CO2). We studied the effects of CO2 on eCPP and ZFP in 17 healthy volunteers. After baseline measurements of middle cerebral artery blood-flow velocity and blood pressure, subjects voluntarily hyperventilated to decrease their end-tidal CO2 (P E′co2) by approximately 7.5 mm Hg, and then they increased their P E′co2 by approximately 7.5 mm Hg by breathing through a Mapleson D circuit. Blood-flow velocity and blood pressure were recorded at each stage. The eCPP and ZFP were calculated by using established formulas, and the results were analyzed with analysis of variance. With increasing P E′co2, eCPP increased from 50.67 mm Hg (8.33 mm Hg) (mean [sd]) to 60.87 mm Hg (9.28 mm Hg) (20% increase;P < 0.001), with a corresponding decrease in ZFP (P = 0.017); hypocapnia resulted in the opposite effects on eCPP and ZFP. These results indicate physiological changes in eCPP and ZFP that can be expected from changes in CO2 in subjects without any neurological disorder. |
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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 |
ISSN: | 0003-2999 |
DOI: | 10.1213/01.ANE.0000047273.85729.A7 |