Reduced fetal movement (RFM) is commonly defined as any reduction in maternal perception of fetal activity. Perceived fetal activity may be movement of limbs, trunk or head movement, but excludes fetal hiccoughs (as this is involuntary movement). The perception of fetal movement by an expectant mother is the first, and ongoing, non-sonographic indicator of fetal viability. The “normal” pattern of fetal movements varies from pregnancy to pregnancy, and often does not become established until 28 weeks’ gestation. Many babies have particularly active periods of the day, usually corresponding to periods of maternal rest and inactivity (which may in itself reflect increased maternal awareness of fetal movement). A variable percentage of sonographically observed fetal movements are perceived by prospective mothers (commonly 30–40%, although some studies report rates as high as 80%).

Healthy pregnancy is characterised by progressive physiological adaptation of the maternal cardiovascular (CV) system that facilitates optimal fetal development. The adaptations that constitute a healthy or normal progression are not always evident, and, in particular, CV adaptation to pregnancy is highly individualised. Some women develop pregnancy-related CV dysfunction such as pre-eclampsia (PE). Typically, PE is diagnosed by the development of hypertension and proteinuria after 20 weeks of pregnancy and is the leading cause of maternal and perinatal mortality and morbidity. Despite continued efforts to improve the understanding of the aetiology, pathophysiology and subsequently treatment for the disease, CV changes in PE are not well understood. PE before 34 weeks (early onset PE) is believed to differ in pathogenesis from late onset PE (>34 weeks) and can be characterised by a haemodynamic profile of increased systemic vascular resistance (SVR) and lower cardiac output (CO). Early onset PE is more often associated with uteroplacental insufficiency and significant adverse maternal and perinatal outcomes. In contrast, late onset PE (>34 weeks) involves an increased CO and lower SVR and is less likely to be associated with uteroplacental insufficiency and adverse perinatal outcomes. It is not known if PE develops secondary to the CV maladaptation in pregnancy or if a preexisting CV dysfunction predisposes some women to develop PE. Screening, diagnosis and disease management would be vastly improved if more were known about the onset of the maladaptive process associated with PE. To date, a combination of maternal factors including medical history, body mass index, age, parity and blood pressure (BP) have been used to predict the development of PE. In the first trimester, arterial stiffness is significantly increased in women who develop PE. Current hypotheses speculate that CV dysfunction is evident very early in pregnancy in PE and precedes the clinical manifestation at a later stage but whether CV dysfunction is present before pregnancy remains to be elucidated.