TY - JOUR
T1 - Transcranial Doppler sonographic measurements of middle cerebral artery flow velocity during hyperbaric oxygen exposures
AU - Visser, G. H.
AU - van Hulst, R. A.
AU - Wieneke, G. H.
AU - van Huffelen, A. C.
PY - 1996
Y1 - 1996
N2 - In the present study, experimental exposures to hyperbaric oxygen (HBO2) were performed (30-min exposure to 2.8 bar (280 kPa) pure oxygen). During all phases of the experiment, blood flow velocity in the right middle cerebral artery was monitored with transcranial Doppler (TCD) sonography. Time courses of heart rate, blood pressure, respiratory rate, end-tidal CO2, and TCD mean velocity (Vmean) are described for a group of 23 subjects during uncomplicated exposure to HBO2 and for three subjects who showed signs of central nervous system (CNS) O2 toxicity, including one subject with a HBO2-induced generalized tonic-clonic seizure. Hyperbaric oxygen decreased Vmean an effect that could not completely be explained by changes in end-tidal CO2. The findings of the present study are in agreement with the concept that an increase in partial oxygen pressure is the primary factor underlying CNS O2 toxicity. Of the variables analyzed, the TCD Vmean is the most valuable variable for monitoring a HBO2 exposure. The Vmean showed the most pronounced change during HBO2 application, and in one subject a sudden increase in Vmean during HBO2 exposure heralded toxicity before clinical signs. It should be realized, however, that the small series of subjects with toxicity in this study does not allow us to draw definite conclusions
AB - In the present study, experimental exposures to hyperbaric oxygen (HBO2) were performed (30-min exposure to 2.8 bar (280 kPa) pure oxygen). During all phases of the experiment, blood flow velocity in the right middle cerebral artery was monitored with transcranial Doppler (TCD) sonography. Time courses of heart rate, blood pressure, respiratory rate, end-tidal CO2, and TCD mean velocity (Vmean) are described for a group of 23 subjects during uncomplicated exposure to HBO2 and for three subjects who showed signs of central nervous system (CNS) O2 toxicity, including one subject with a HBO2-induced generalized tonic-clonic seizure. Hyperbaric oxygen decreased Vmean an effect that could not completely be explained by changes in end-tidal CO2. The findings of the present study are in agreement with the concept that an increase in partial oxygen pressure is the primary factor underlying CNS O2 toxicity. Of the variables analyzed, the TCD Vmean is the most valuable variable for monitoring a HBO2 exposure. The Vmean showed the most pronounced change during HBO2 application, and in one subject a sudden increase in Vmean during HBO2 exposure heralded toxicity before clinical signs. It should be realized, however, that the small series of subjects with toxicity in this study does not allow us to draw definite conclusions
M3 - Article
C2 - 8931283
SN - 1066-2936
VL - 23
SP - 157
EP - 165
JO - Undersea & hyperbaric medicine
JF - Undersea & hyperbaric medicine
IS - 3
ER -