DISCUSSION
8.2 Prognostic value of haemodynamic studies
8.2.2. Limitations of maternal haemodynamics studies
Our study shows that the uterine artery resistance index measured at late second or early third trimesters, probably encompasses all the known risk variables such as severity and chronicity of hypertension, presence and severity of proteinuria, and possibly also bad obstetric history, multiparity, higher age, and maternal size. It proved to be the best single variable to correlate with adverse feto-neonatal outcome.
These findings are supported by recent observations made by Frusca et al, (2003) in their retrospective study evaluating uterine artery velocimetry in women with gestational hypertension and pre-eclampsia. In a multivariate model that looked at presence of proteinuria, severity of hypertension and uterine artery velocimetry, the authors found that abnormal uterine velocimetry was the variable that was more frequently associated with adverse pregnancy outcome.
neonatal outcome. One of several conclusions made by the authors was that a failure to adjust antihypertensive medication in response to an excessive drop in cardiac output or a corresponding increase in systemic vascular resistance was associated with an increased risk of fetal growth restriction. Apart from being a retrospective
analysis, the arbitrary cut-off value for cardiac output (without stratifying for maternal size) and the inclusion of normotensive patients with a history of fetal growth
restriction are significant limitations in this study.
The more conclusive work of Bosio et al, (1999) described an elevated maternal cardiac output in the pre-clinical period of normotensive women who developed hypertension later in pregnancy. Their data supports the hypothesis of a hyperdynamic disease model in women with pre-eclampsia and gestational aproteinuric
hypertension. However, again this study did not correlate cardiac output to maternal body size (normalised BSA). Earlier studies have shown a poor correlation of maternal cardiac output with maternal body size, but in our study of normotensive pregnant there is women show a significant positive correlation between maternal cardiac output and maternal body size. In addition our study together with that of Bosio et al, (1999) show a very satifactory feto-neonatal outcome in women who present with gestational hypertension late in pregnancy. These patients have normal cardiac output with mildly elevated systemic vascular resistance late in pregnancy, supporting the concept that the elevated cardiac output in the pre-clinical phase of the disease is followed by a reduction in cardiac output in the clinical phase of disease (pre-eclampsia). This highlights the limitation of a single measure of cardiac output to risk stratify pre-eclamptic women. It can probably be stated that if increased cardiac index is indeed a feature of the initial stages of pre-eclampsia, then the results
of our study suggest that this does not persist into the clinical stage of the disease when cardiac index may be within the normal range but systemic vascular resistance index is high.
Our study evaluated women in the clinical phase of pre-eclampsia with the aim of providing more precise risk stratification. We show a trend to a lower cardiac output in a smaller sample of preeclamptic women compared to normotensives (p = 0.116) that corresponded to significant differences in feto-neonatal outcome. The lower cardiac output in our preeclamptic group compared to chronic hypertension with superimposed pre-eclampsia was not associated with a more adverse feto-neonatal outcome. Standardizing maternal cardiac output for maternal body size (body surface area) in our study revealed no differences in cardiac index among the hypertensive groups. These data suggest that, if indeed a reduced cardiac output is a marker of adverse feto-neonatal outcome, then there must be compensatory mechanisms, probably at uteroplacental level, to maintain satifactory fetal health. Our study thus provides supporting evidence for this hypothesis since there was poor correlation of maternal central hemodynamics compared to uterine artery velocimetry with adverse feto-neonatal outcome in hypertensive pregnancies.
The modest to poor correlation of maternal haemodynamic parameters with uterine artery resistance index, and the fact that the echocardiographic Doppler technique is labour and skills intensive - shows that risk stratifying hypertensive pregnancies by Doppler measurement of uterine artery resistance index is a more rewarding approach.
Yang et al, (1996), has shown that women with systemic vascular resistance index in the upper textile had a higher incidence of small for gestational age babies. Similar to most studies of maternal hemodynamics in hypertensive pregnancies, the authors reported the limitations that arise as a result of a large variability in cardiac index.
They observed that the pre-eclamptic sub-group had an elevated uterine artery
resistance without a corresponding reduction in cardiac output or significant elevation of systemic vascular resistance index. This suggests that the relationship between regional uterine hemodynamics and maternal central hemodynamics is not linear in hypertensive pregnancies and it is likely that uteroplacental vasospasm occurs before systemic vasospasm. These authors hypothesized that an elevated cardiac output in these pre-eclamptic women reflected a hyperdynamic circulation that may be compensatory to maintain adequate perfusion in a high resistance utero-placental circulation.
Two studies using bioimpedance have evaluated the responses to volume expansion in pre-eclampsia. Siekmann et al, (1986) found that hypervolemic hemodilution with dextran in pre-eclampsia correlated with a rise in fetal blood flow velocity and flow volume and proposed that elevation in uteroplacental perfusion occurred as a result of an increase in maternal cardiac output. Subsequently Belfort et al, (1994) evaluated maternal hemodynamics by thoracic electrical bioimpedance and simultaneous uterine artery Doppler in five preeclamptics who received volume expansion followed by verapamil infusion. The authors noted widely varying changes in cardiac index but either unchanged or improved measurement in uterine artery velocimetry indices and the authors concluded that volume expansion could have limited benefits in such patients.
8.2.3 Clinical limitations: effects of treatment and maternal body habitus