Noninvasive Estimation of Cerebral Perfusion Pressure and Zero Flow Pressure in Healthy Volunteers: The Effects of Changes in End-Tidal Carbon Dioxide

In addition to cerebrovascular resistance (CVR) zero flow pressure (ZFP), effective cerebral perfusion pressure (CPPe) and the resistance area product (RAP) are supplemental determinants of cerebral blood flow (CBF). Until now, the interrelationship of PaCO2 -induced changes in CBF, CVR, CPPe, ZFP, and RAP is not fully understood. In a controlled crossover trial, we investigated 10 anesthetized patients aiming at PaCO2 levels of 30, 37, 43, and 50 mm Hg. Cerebral blood flow was measured with a modified Kety-Schmidt-technique. Zero flow pressure and RAP was estimated by linear regression analysis of pressure–flow velocity relationships of the middle cerebral artery. Effective cerebral perfusion pressure was calculated as the difference between mean arterial pressure and ZFP, CVR as the ratio CPPe/CBF. Statistical analysis was performed by one-way RM-ANOVA. When comparing hypocapnia with hypercapnia, CBF showed a significant exponential reduction by 55% and mean VMCA by 41%. Effective cerebral perfusion pressure linearly decreased by 17% while ZFP increased from 14 to 29 mm Hg. Cerebrovascular resistance increased by 96% and RAP by 39%; despite these concordant changes in mean CVR and Doppler-derived RAP correlation between these variables was weak ( r = 0.43). In conclusion, under general anesthesia hypocapnia-induced reduction in CBF is caused by both an increase in CVR and a decrease in CPPe, as a consequence of an increase in ZFP.

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The effect of respiratory physiotherapy on intracranial pressure, mean arterial pressure, cerebral perfusion pressure and end tidal carbon dioxide in ventilated neurosurgical patients

Physiotherapy Theory and Practice ◽

10.3109/09593989309036480 ◽

1993 ◽

Vol 9 (1) ◽

pp. 3-11 ◽

Cited By ~ 21

Author(s):

Jennifer Paratz ◽

Yvonne Burns

Keyword(s):

Carbon Dioxide ◽

Mean Arterial Pressure ◽

Intracranial Pressure ◽

Arterial Pressure ◽

Cerebral Perfusion ◽

Perfusion Pressure ◽

Neurosurgical Patients ◽

End Tidal Carbon Dioxide ◽

Respiratory Physiotherapy ◽

End Tidal

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The Effects of Propofol or Sevoflurane on the Estimated Cerebral Perfusion Pressure and Zero Flow Pressure

Anesthesia & Analgesia ◽

10.1213/01.ane.0000146522.84181.d3 ◽

2005 ◽

Vol 100 (3) ◽

pp. 835-840 ◽

Cited By ~ 30

Author(s):

Paul D. Marval ◽

Mandy E. Perrin ◽

Sally M. Hancock ◽

Ravi P. Mahajan

Keyword(s):

Cerebral Perfusion Pressure ◽

Cerebral Perfusion ◽

Perfusion Pressure ◽

Flow Pressure ◽

Zero Flow

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The Effects of Propofol or Sevoflurane on the Estimated Cerebral Perfusion Pressure and Zero Flow Pressure

Survey of Anesthesiology ◽

10.1097/01.sa.0000185358.68694.9c ◽

2005 ◽

Vol 49 (6) ◽

pp. 309

Author(s):

&NA;

Keyword(s):

Cerebral Perfusion Pressure ◽

Cerebral Perfusion ◽

Perfusion Pressure ◽

Flow Pressure ◽

Zero Flow

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Phase I Safety Assessment of Intrathecal Neostigmine Methylsulfate in Humans

Anesthesiology ◽

10.1097/00000542-199502000-00003 ◽

1995 ◽

Vol 82 (2) ◽

pp. 331-343 ◽

Cited By ~ 180

Author(s):

David D. Hood ◽

James C. Eisenach ◽

Robin Tuttle

Keyword(s):

Carbon Dioxide ◽

Blood Pressure ◽

Heart Rate ◽

Side Effects ◽

Healthy Volunteers ◽

Nausea And Vomiting ◽

Severe Nausea ◽

End Tidal Carbon Dioxide ◽

End Tidal ◽

Ice Water

Background In dogs, sheep, and rats, spinal neostigmine produces analgesia alone and enhances analgesia from alpha 2-adrenergic agonists. This study assesses side effects and analgesia from intrathecal neostigmine in healthy volunteers. Methods After institutional review board approval and informed consent, 28 healthy volunteers were studied. The first 14 volunteers received neostigmine (50-750 micrograms) through a #19.5 spinal needle followed by insertion of a spinal catheter. The remaining 14 volunteers received neostigmine through a #25 or #27 spinal needle without a catheter. Safety measurements included blood pressure, heart rate, oxyhemoglobin saturation, end-tidal carbon dioxide, neurologic evaluation, and computer tests of vigilance and memory. Analgesia in response to ice water immersion was measured. Results Neostigmine (50 micrograms) through the #19.5 needle did not affect any measured variable. Neostigmine (150 micrograms) caused mild nausea, and 500-750 micrograms caused severe nausea and vomiting. Neostigmine (150-750 micrograms) produced subjective leg weakness, decreased deep tendon reflexes, and sedation. The 750-micrograms dose was associated with anxiety, increased blood pressure and heart rate, and decreased end-tidal carbon dioxide. Neostigmine (100-200 micrograms) in saline, injected through a #25 or #27 needle, caused protracted, severe nausea, and vomiting. This did not occur when dextrose was added to neostigmine. Neostigmine by either method of administration reduced visual analog pain scores to immersion of the foot in ice water. Conclusions The incidence and severity of these adverse events from intrathecal neostigmine appears to be affected by dose, method of administration, and baricity of solution. These effects in humans are consistent with studies in animals. Because no unexpected or dangerous side effects occurred, cautious examination of intrathecal neostigmine alone and in combination with other agents for analgesia is warranted.

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