title: Cerebral haemodynamics in pregnancy and pre-eclampsia as assessed by transcranial Doppler ultrasonography.
abstract: BACKGROUND
  Altered cerebral circulation, as reported during normal pregnancy, and in patients with pre-eclampsia, can be associated with changes in cerebral vascular reactivity and/or cerebral autoregulation. The aim of our study was to perform a comparative assessment of cerebral haemodynamics, including vascular reactivity and autoregulation, in pre-eclamptic patients, healthy pregnant women, and healthy non-pregnant women.
  
  
  METHODS
  Thirty patients with pre-eclampsia were recruited. Age- and height-matched healthy pregnant (n=30) and non-pregnant control (n=30) groups were also recruited. Monitoring included transcranial Doppler ultrasonography, end-tidal carbon dioxide and non-invasive arterial pressure measurement. Cerebral autoregulation was assessed by performing the transient hyperaemic response (THR) test. The cerebrovascular reactivity to carbon dioxide (CRCO(2)) was assessed by measuring middle cerebral artery blood flow velocity (MCAFV) after induced changes in end-tidal carbon dioxide. Estimated cerebral perfusion pressure (eCPP) and critical closing pressure (CrCP) were calculated using established formulae. Statistical analysis included ANOVA with Tukey's pairwise comparisons.
  
  
  RESULTS
  Mean arterial pressure (MAP) was increased in pre-eclampsia (P<0.05). Mean MCAFV was lower in healthy pregnancy (P<0.05), but in pre-eclampsia it was similar to the non- pregnant group. When compared with the non-pregnant group, mean eCPP was higher in the healthy pregnant and pre-eclamptic groups (P<0.05). There were no meaningful differences in cerebral autoregulation or CRCO(2).
  
  
  CONCLUSIONS
  Healthy pregnancy increases eCPP, presumably by decreasing CrCP. In pre-eclampsia, eCPP is maintained at the same level as in healthy pregnancy despite an increased MAP. Pre-eclampsia has no significant effect on cerebral autoregulation or CRCO(2).
authors.affiliation: University Department of Anaesthesia, Nottingham City Hospital, Nottingham NG5 1PB, UK.
authors.forename: R W
authors.initials: RW
authors.lastname: Sherman
authors.forename: R A
authors.initials: RA
authors.lastname: Bowie
authors.forename: M M E
authors.initials: MM
authors.lastname: Henfrey
authors.forename: R P
authors.initials: RP
authors.lastname: Mahajan
authors.forename: D
authors.initials: D
authors.lastname: Bogod
mesh_terms: D000293:Adolescent; D000328:Adult; D001783:Blood Flow Velocity / Q000502:physiology; D001794:Blood Pressure / Q000502:physiology; D002245:Carbon Dioxide / Q000502:physiology; D002560:Cerebrovascular Circulation / Q000502:physiology*; D005260:Female; D006706:Homeostasis; D006801:Humans; D008875:Middle Aged; D011225:Pre-Eclampsia / Q000000981:diagnostic imaging / Q000503:physiopathology*; D011247:Pregnancy / Q000502:physiology*; D017585:Ultrasonography, Doppler, Transcranial
chemical_list: D002245:Carbon Dioxide