AMNIOTIC-FLUID INDEX AND MEAN DIASTOLIC MATERNAL BLOOD-PRESSURE IN PREGNANCY-INDUCED HYPERTENSIVE PATIENTS

Citation
H. Valensise et al., AMNIOTIC-FLUID INDEX AND MEAN DIASTOLIC MATERNAL BLOOD-PRESSURE IN PREGNANCY-INDUCED HYPERTENSIVE PATIENTS, Hypertension in pregnancy, 15(2), 1996, pp. 219-228
Citations number
27
Categorie Soggetti
Obsetric & Gynecology","Cardiac & Cardiovascular System",Physiology
Journal title
ISSN journal
10641955
Volume
15
Issue
2
Year of publication
1996
Pages
219 - 228
Database
ISI
SICI code
1064-1955(1996)15:2<219:AIAMDM>2.0.ZU;2-C
Abstract
Objective: To determine the correlation between maternal blood pressur e value and the volume of amniotic fluid. Methods: Amniotic fluid inde x (AFI) and fetal and maternal Doppler, followed by 24-h ambulatory bl ood pressure were determined in patients with preeclampsia (n = 10), g estational hypertension patients (n = 28), fetal growth retardation (I UGR) (n = 23); and with a healthy normotensive pregnancy (n = 39). Mea n 24-h diastolic blood pressure (M24h DBP) was used to describe the ov erall pressure regimen for each patient. Uteroplacental resistance and fetal peripheral resistance were investigated through color Doppler e valuation of the uterine, umbilical, and middle cerebral arteries. Res ults: A significant inverse linear correlation between AFI values and M24h DBP was found for the patients with gestational hypertension (r = -0.45, P < 0.005). In the patients with normal uterine resistance (RI ), normal fetal growth, and normal Doppler indexes there was a stronge r negative correlation (r = -0.66, P < 0.001). No correlation between AFI and M24h DBP was seen in patients with preeclampsia or in those wi th IUGR, where a redistribution of blood flow with a reduced perfusion of the splanchnic organs was found (umbilical/middle cerebral artery ratio was higher than in the control group, P < 0.001). Conclusions: I n gestational hypertensive patients with no sign of fetal distress, th e inverse correlation between AFI and mean 24-h diastolic blood pressu re cannot be explained with the redistribution of fetal blood flow. An underlying pathophysiological mechanism involving changes in intracel lular electrolyte balance may be responsible for hypertension and AFI reduction.