Research has shown that some pregnancy induced hypertension (PIH) cases had prior undetected hypertension. For example, a kidney biopsy 6 months postpartum (when all PIH induced morphologic changes have normally subsided in idiopathic PIH cases) revealed that 65.5% of PIH patients actually had renal disease. A 1978-1980 study showed risk factors to include nulliparity, increasing age, black race, multiple gestations, concomitant heart or renal disease, and chronic hypertension. Even though physicians have depended on screening for elevated blood pressures in the 2nd trimester to hedge eclampsia, a study demonstrated that only 8.7% of nulliparas with diastolic blood pressure 80 mm Hg and none 90 mm Hg developed eclampsia. Pathogenesis of PIH appears to be reduced uteroplacental perfusion. This reduction may be caused by disturbed prostaglandin relationships, increased placental production of progesterone, increased amounts of atrial natriuretic peptide, or increased amounts of a digoxin like immunoreactive substance that inhibits the sodium-potassium ATPase pump. Traditional treatment for PIH consists of bed rest, nutritious diet, and hypertensive drugs. A controlled study revealed, however, that drug therapy of maternal blood pressure did not change perinatal outcome and increased fetal growth retardation. Oral contraceptives (OCs) may induce high blood pressure in women 35 years old, smokers, and obese women. This can be managed by using the following guidelines: using the lowest effective OC dose of estrogen and progestin, providing a 6 month supply, monitoring blood pressure frequently, and discontinuing OC use if blood pressure rise 10/5 mm Hg. Postmenopausal hormonal replacement therapy decreases the risk of vascular diseases and does not affect blood pressure.
|Original language||English (US)|
|Number of pages||8|
|State||Published - Dec 1 1988|
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine