Significant hypertension must be treated in its own right, regardless of the assumed underlying pathology, largely to reduce the risk of maternal intracranial hemorrhage.
The level at which antihypertensive treatment is initiated for nonsevere hypertension remains controversial, depending on whether treatment is focused on maternal or fetal wellbeing. Most physicians commence antihypertensive medication when the systolic blood pressure > 140-170 mm Hg or diastolic pressure > 90-110 mm Hg. Treatment is mandatory for severe hypertension when the blood pressure is 170/110 mm Hg. Once treatment is started, target blood pressure is also controversial, but many practitioners would treat to keep the mean arterial pressure < 125 mm Hg—for example, a blood pressure of 150/100 mm Hg. Overzealous blood pressure control may lead to placental hypoperfusion, as placental blood flow is not autoregulated, and this will compromise the fetus. Unfortunately there is no evidence that pharmacological treatment of chronic or gestational hypertension protects against the development of preeclampsia. Changes in diet or bed rest have not been shown to provide maternal or fetal benefit.
All antihypertensive drugs have either been shown, or are assumed, to cross the placenta and reach the fetal circulation. However, as previously stated, none of the C antihypertensive agents in routine use have been documented to be teratogenic, although ACE inhibitors and ARBs are fetotoxic. The objective of treating hyper-tension in pregnancy is to protect the woman from C/9 dangerously high blood pressure and to permit continuation of the pregnancy, fetal growth and maturation.
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