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 inAnesthesia and analgesia Vol. 96; no. 3; pp. 847 - 851
Main Authors Hancock, Sally M., Mahajan, Ravi P., Athanassiou, Labros
Format Journal Article
LanguageEnglish
Published Hagerstown, MD International Anesthesia Research Society 01.03.2003
Lippincott
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Abstract 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.
AbstractList 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 (CO(2)). We studied the effects of CO(2) 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 CO(2) (PE'CO(2)) by approximately 7.5 mm Hg, and then they increased their PE'CO(2) 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 PE'CO(2), 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 CO(2) in subjects without any neurological disorder. Increasing end-tidal CO(2) increases the estimated cerebral perfusion pressure and vice versa. These results are opposite to those expected from the known effects of CO(2) on intracranial pressure. Thus, we support the suggestion that, in the absence of intracranial hypertension, vascular tone remains a major determinant of effective downstream pressure and cerebral perfusion.
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.
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 (CO(2)). We studied the effects of CO(2) 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 CO(2) (PE'CO(2)) by approximately 7.5 mm Hg, and then they increased their PE'CO(2) 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 PE'CO(2), 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 CO(2) in subjects without any neurological disorder.UNLABELLEDZero 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 (CO(2)). We studied the effects of CO(2) 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 CO(2) (PE'CO(2)) by approximately 7.5 mm Hg, and then they increased their PE'CO(2) 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 PE'CO(2), 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 CO(2) in subjects without any neurological disorder.Increasing end-tidal CO(2) increases the estimated cerebral perfusion pressure and vice versa. These results are opposite to those expected from the known effects of CO(2) on intracranial pressure. Thus, we support the suggestion that, in the absence of intracranial hypertension, vascular tone remains a major determinant of effective downstream pressure and cerebral perfusion.IMPLICATIONSIncreasing end-tidal CO(2) increases the estimated cerebral perfusion pressure and vice versa. These results are opposite to those expected from the known effects of CO(2) on intracranial pressure. Thus, we support the suggestion that, in the absence of intracranial hypertension, vascular tone remains a major determinant of effective downstream pressure and cerebral perfusion.
Author Mahajan, Ravi P.
Hancock, Sally M.
Athanassiou, Labros
AuthorAffiliation University Departments of Anaesthesia and Intensive Care, Queen’s Medical Centre and City Hospital NHS Trust, Nottingham, United Kingdom
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Issue 3
Keywords Human
Healthy subject
Carbon dioxide
Central nervous system
Intracranial pressure
Pressure
Blood flow
Expired gas
Hypercapnia
Perfusion
Hypocapnia
Arterial pressure
Hemodynamics
Brain (vertebrata)
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Snippet Zero flow pressure (ZFP) in the cerebral circulation is defined as the arterial pressure at which flow ceases. Noninvasive methods of estimating cerebral...
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SubjectTerms Adult
Algorithms
Biological and medical sciences
Blood Pressure - physiology
Brain
Carbon Dioxide - blood
Carbon Dioxide - metabolism
Carbon Dioxide - pharmacology
Cerebrovascular Circulation - physiology
Female
Humans
Hypercapnia - physiopathology
Investigative techniques of hemodynamics
Investigative techniques, diagnostic techniques (general aspects)
Male
Medical sciences
Middle Aged
Middle Cerebral Artery - physiology
Title Noninvasive Estimation of Cerebral Perfusion Pressure and Zero Flow Pressure in Healthy Volunteers: The Effects of Changes in End-Tidal Carbon Dioxide
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