TY - JOUR
T1 - Concurrent increases in brain electrical activity and intracranial blood flow velocity during low-dose ketamine anaesthesia
AU - Kochs, Eberhard
AU - Werner, Christian
AU - Hoftman, William E.
AU - Möllenberg, Oliver
AU - Schulte am Esch, Jochen
PY - 1991/10
Y1 - 1991/10
N2 - The purpose of the present study was to assess the effects of low-dose ketamine on spontaneous brain electrical activity (EEG) and intracranial blood flow velocity. Twenty healthy volunteers were divided into two groups: Group I (n=10) received 0.25 mg·kg-1 ketamine iv; Group II (n=10) received 0.5 mg·kg-1 ketamine iv. Mean arterial blood pressure (MAP), heart rate (HR), end-tidal PCO2 (P etCO2), and arterial oxygen saturation (SaO2) were measured. The EEG was recorded from temporo-occipital recording sites over both hemispheres. Blood flow velocity in the middle cerebral artery was measured using a transcranial Doppler ultrasound system. All variables were evaluated at baseline and for 60 min following ketamine. Administration of ketamine resulted in increases of MAP and HR in both groups to a similar degree. The PetCO2 and SaO2 did not change in either group over time. Ketamine caused a dose-dependent, transient shift in the EEG to synchronous high-voltage slow waves with an increase in total power (Group 1: 301±38%; Group II: 104±28%). These changes were associated with dose-dependent increases in mean blood flow velocity (Group I: 35±7%; Group II: 68±10%). Our data suggest that increases in intracranial blood flow velocity are closely correlated to increases in neuronal activity and are not secondary to changes in systemic haemodynamic variables.
AB - The purpose of the present study was to assess the effects of low-dose ketamine on spontaneous brain electrical activity (EEG) and intracranial blood flow velocity. Twenty healthy volunteers were divided into two groups: Group I (n=10) received 0.25 mg·kg-1 ketamine iv; Group II (n=10) received 0.5 mg·kg-1 ketamine iv. Mean arterial blood pressure (MAP), heart rate (HR), end-tidal PCO2 (P etCO2), and arterial oxygen saturation (SaO2) were measured. The EEG was recorded from temporo-occipital recording sites over both hemispheres. Blood flow velocity in the middle cerebral artery was measured using a transcranial Doppler ultrasound system. All variables were evaluated at baseline and for 60 min following ketamine. Administration of ketamine resulted in increases of MAP and HR in both groups to a similar degree. The PetCO2 and SaO2 did not change in either group over time. Ketamine caused a dose-dependent, transient shift in the EEG to synchronous high-voltage slow waves with an increase in total power (Group 1: 301±38%; Group II: 104±28%). These changes were associated with dose-dependent increases in mean blood flow velocity (Group I: 35±7%; Group II: 68±10%). Our data suggest that increases in intracranial blood flow velocity are closely correlated to increases in neuronal activity and are not secondary to changes in systemic haemodynamic variables.
KW - Anaesthetics, Intravenous: ketamine
KW - Brain: blood flow velocity, elctroencephalography
KW - Measurement Techniques: Doppler ultrasound, transcranial
UR - http://www.scopus.com/inward/record.url?scp=0025994804&partnerID=8YFLogxK
U2 - 10.1007/BF03036955
DO - 10.1007/BF03036955
M3 - Article
C2 - 1742815
AN - SCOPUS:0025994804
SN - 0832-610X
VL - 38
SP - 826
EP - 830
JO - Canadian Journal of Anesthesia
JF - Canadian Journal of Anesthesia
IS - 7
ER -