PATHOPHYSIOLOGY AND HEMODYNAMIC RESPONSE TO PREGNANCY INDUCED HYPERTENSION AND FETAL HYPOXIA

PATHOPHYSIOLOGY AND HEMODYNAMIC RESPONSE TO PREGNANCY INDUCED HYPERTENSION AND FETAL HYPOXIA

          Despite extensive research, the exact cause of pre-eclampsia remains unknown and it has been aptly referred to as the ‘disease of theories’ (Rubin et aL1994). But there are histological evidences which prove that the pathogenesis of the disease involves abnormal development of small uterine vessels. There is incomplete or absence of trophoblastic invasion of the spiral arteries (Gerresten et al 1981; Redman, 1991).

          There is further evidence that vasospasm is basic to PIH. It involves the arterioles of the uteroplacenta circulation, kidneys, eyes and other organs, which may be due to the imbalance in placental prostacyclin and thromboxane production (Walsh, 1985).

Uterine Arteries in PIH:

          Uterine artery blood flow reflects hemodynamic changes that occur at the maternal side of the placenta (Trudinger et al 1985). These physiologic changes of the placental bed spiral arteries extend only to the deciduc myometrial junction. In pre-eclampsia the spiral arteries may remain unconverted throughout their decidual and myometrial length.

          Another placental bed lesion seen with preeclampsia is an acute arteriopathy, termed acute atherosis. These lesions are seen in the deciduat and myometrial segments of the placental bed spiral arteries, which have not undergone physiologic changes. The breadth and the severity of the lesion correlates with the severity and the duration of hypertension (Zeek et aL, 1950).

          The umbilical arteries are not innervated, beyond the proximal 1-2 cm of the umbilical cord, Acute hypoxemia does not change the magnitude of umbilical-placental blood flow, suggesting that hypoxemia has little or no direct effect on the umbilical-placental circulation (Peeters et al 1979).

          However, umbilical flow may be altered by hypoxemia secondary to changes in arterial blood pressure, fetal heart rate. Although total umbilical-placental blood flow does not change during hypoxia, the total vascular resistance to flow increases significantly (Paijljk et al,, 1990),

Fetal Cerebral Circulation in PIH:

          Oxygen crosses the placenta through a process of facilitated diffusion. As the number of arterioles in the tertiary stem villi is decreased in PIH, the total surface area for diffusion is also decreased. As a result, there is reduced transfer of oxygen and nutrients to the fetus across the placenta. The first response of a fetus faced with a reduced supply of nutrients from the placenta is to reduce its metabolic needs by slowing growth velocity.

          There is preferential shift of cardiac output in favour of the left ventricle, leading to improved perfusion of the brain and heart at the expense of the rest of the body. In the middle cerebral artery, significant vaso-dilatation was observed in response to fetaljhypoxia mediated by chemoreceptors (Arbeille et at, 1995).

          Further deterioration of fetal oxygen supply leads to ‘acidosis’

SEQUENCE OF CHANGES IN FETAL CIRCULATION IN PIH LEADING TO HYPOXEMIA

          Fetal circulation undergoes a sequence of changes in response to hypoxemia. The initial response observed with Doppler ultrasound is cerebral vascular dilatation. This encourages an increased flow of blood with the highest oxygen concentration to the developing fetal brain. Venous Doppler studies become abnormal at a later stage. The increased after load, especially on the right side of the heart ultimately manifest in the changes seen in the inferior vena cava, ductus venosus and hepatic veins.