Cerebral autoregulation in normal pregnancy and preeclampsia.

Obstet Gynecol

University Medical Center Groningen, Department of Obstetrics and Gynecology, Groningen, the Netherlands; Baylor College of Medicine, Department of Obstetrics and Gynecology, Houston, Texas; University of Leicester, Department of Cardiovascular Sciences, Leicester, United Kingdom; St. David's Women's Center of Texas, North Austin Maternal-Fetal Medicine, Austin, Texas; and Erasmus Medical Center, Department of Obstetrics and Gynecology, Rotterdam, the Netherlands.

Published: November 2013

Objective: To test the hypothesis that preeclampsia is associated with impaired dynamic cerebral autoregulation.

Methods: In a prospective cohort analysis, cerebral blood flow velocity of the middle cerebral artery (determined by transcranial Doppler), blood pressure (determined by noninvasive arterial volume clamping), and end-tidal carbon dioxide were simultaneously collected during a 7-minute period of rest. The autoregulation index was calculated. Values of 0 and 9 indicated absent and perfect autoregulation, respectively. Student t test was used, with P<.05 considered significant.

Results: Women with preeclampsia (before treatment, n=20) and their normotensive counterparts (n=20) did not differ with respect to baseline characteristics, except for earlier gestational age at delivery (36 3/7 [24 4/7-40 2/7] compared with 39 2/7 [32 0/7-41 0/7]; P<.001) and higher blood pressure in women with preeclampsia. Autoregulation index was significantly reduced in preeclamptic women compared with normotensive women in the control group (5.5±1.7 compared with 6.7±0.6; P=.004). There was no correlation between the autoregulation index and blood pressure.

Conclusion: Women with preeclampsia have impaired dynamic cerebral autoregulation. The fact that blood pressure does not correlate with autoregulation functionality may explain why cerebral complications such as eclampsia can occur without sudden or excessive elevation in blood pressure.

Level Of Evidence: II.

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Source
http://dx.doi.org/10.1097/AOG.0b013e3182a93fb5DOI Listing

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