Hypertension in pregnancy affects the mother and new-born to varying degrees. Given the characteristic multi-system effects, it is clear that several pathophysiologic mechanisms are involved (Fig. 16.1). The predominant patho-physiologic finding in preeclampsia and gestational hypertension is maternal vasospasm.Several potential causes for mater-nal vasospasm have been postulated:
· Vascular changes: Instead of noting the physiologictrophoblast-mediated vascular changes in the uterine vessels (decreased musculature in the spiral arterioles leads to the development of a low-resistance, low-pressure, high-flow system), inadequate maternal vas-cular response is seen in cases of preeclampsia and/or intrauterine fetal growth restriction. Endothelial dam-age is also noted within the vessels.
· Hemostatic changes: Increased platelet activationwith increased consumption in the microvasculature is noted during the course of preeclampsia. Endothelial fibronectin levels are increased and antithrombin III and α2-antiplasmin levels are decreased, reflecting en-dothelial damage. Low antithrombin III levels are per-missive for microthrombi development. Endothelial damage is then thought to promote further vasospasm.
· Changes in prostanoids: Prostacyclin (PGI2) andthromboxane (TXA2) are increased during pregnancy, with the balance in favor of PGI2. In patients who develop preeclampsia, the balance shifts to favor TXA2. Again, PGI2 functions to promote vasodilatation and decrease platelet aggregation, and TXA2 promotes vaso-constriction and platelet aggregation. Because of this imbalance, vessel constriction occurs.
· Changes in endothelium-derived factors: Nitricoxide, a potent vasodilator, is decreased in patients with preeclampsia and may explain the evolution of vaso-constriction in these patients.
· Lipid peroxide, free radicals, and antioxidant release: Lipid peroxides and free radicals have been implicated in vascular injury and are increased in pregnancies com-plicated by preeclampsia. Decreased antioxidant levels are also noted.
· These five mechanisms, in any combination or permutation, are thought to contribute to the following common patho-physiologic changes seen in patients with preeclampsia:
· Cardiovascular effects: Elevated blood pressure is seenas the result of potential vasoconstriction as well as an increase in cardiac output.
· Hematologic effects: Plasma volume contractionmay develop, with risk of rapid onset hypovolemic shock, if hemorrhage occurs. Plasma volume con-traction is reflected in increased hematocrit values. Thrombocytopenia/disseminated intravascular coag-ulation may also develop from microangiopathic he-molytic anemia. Involvement of the liver may lead to hepatocellular dysfunction and further evolution of coagulopathy. Third spacing of fluid may be noted, because of increased blood pressure and decreased plasma oncotic pressure.
· Renal effects: Decreased glomerular filtration rate(increasing serum creatinine) and proteinuria (urine protein levels greater than 300 mg per 24 hours) develop secondary to atherosclerotic-like changes in the renal vessels (glomerular endotheliosis). Uric acid filtration is decreased; therefore, elevated maternal serum uric acid levels may be an indication of evolving disease.
· Neurologic effects: Hyperreflexia/hypersensitivity maydevelop. In severe cases, grand mal (eclamptic) seizures may develop.
· Pulmonary effects: Pulmonary edema may occur andcan be related to decreased colloid oncotic pressure, pulmonary capillary leak, left heart failure, iatrogenic fluid overload, or a combination of these factors.
· Fetal effects: Decreased intermittent placental perfu-sion secondary to vasospasm is thought to be responsi-ble for the increased incidence of intrauterine growth restriction (<10% estimated fetal weight for gesta-tional age), oligohydramnios, and increased perinatal mortality of infants born to mothers with preeclamp-sia. An increased incidence of placental abruption is also seen. With the stress of uterine contractions dur-ing labor, the placenta may be unable to adequately oxygenate the fetus. This may result in signs of intra-partum uteroplacental insufficiency. Specifically, a non-reassuring fetal-heart-rate pattern may necessitate cesarean delivery.
Presumably because of vasospastic changes, placental size and func-tion are decreased. The results are progressive fetal hypoxiaand malnutrition, as well as an increase in the incidence of intrauterine growth restriction and oligohydramnios.