Most women with chronic hypertension will have normal healthy pregnancies, especially if the hypertension is mild. Women with stage 1 hypertension (<160/100) who have no evidence of end-organ damage and are otherwise healthy have an excellent prognosis for pregnancy. The primary risk for women in this category is superimposed preeclampsia which occurs in approximately 20 % [5]. Women with severe hypertension (>160/100) have a risk of preeclampsia of 50 %, and women with the most severe disease including those who already have end-organ damage or have a secondary cause of hypertension, have been reported to have a risk of preeclampsia as high as 75 % [4, 10]. The incidence of both maternal and fetal adverse outcomes is related to the duration of disease, severity of disease, and whether or not the mother develops superimposed preeclampsia [11].

Maternal complications are primarily associated with preeclampsia and include a fivefold increase in maternal mortality, as well as an increased risk of maternal cerebrovascular event, pulmonary edema, seizure, and renal failure [12].

Fetal complications include an increased risk of premature birth, intrauterine growth restriction (IUGR), fetal demise, placental abruption, and cesarean delivery [13, 14]. Adverse fetal outcomes are also much more likely in women who develop superimposed preeclampsia [2].

About 5–10 % of women enter pregnancy with a diagnosis of chronic hypertension [5]. In addition, the overwhelming majority of women who have new-onset hypertension prior to 20 weeks gestation will, ultimately, be diagnosed with chronic hypertension. Ideally a woman with chronic hypertension should have a comprehensive evaluation prior to pregnancy. The evaluation of chronic hypertension includes three components: (1) screening for secondary causes, (2) assessment for target organ damage, and (3) a review of cardiovascular risk factors.

Essential hypertension accounts for 90 % of chronic hypertension and is more common in African American women and women who have a family history of hypertension, are obese, or are over 35 years old. If a woman has none of these risk factors, then consideration of secondary causes is important. In addition, any woman with severe refractory hypertension, with sudden escalation of blood pressure, or with specific signs or symptoms should be evaluated for secondary causes (Table 8.2). Although secondary hypertension is rare, it may pose significant risk in pregnancy if undiagnosed.

Target organs that are most commonly affected by chronic hypertension include the heart, the brain, the kidneys, and the eye. Patients should be screened by symptoms, signs, or lab abnormalities (Table 8.3).

All women with hypertension should be screened for other cardiovascular risk factors. In addition to hypertension, independent risk factors for cardiovascular disease in women include obesity (BMI > 30), sedentary lifestyle, hyperlipidemia, diabetes, smoking, end-stage renal disease, a history of gestational hypertension or preeclampsia, and a family history of premature cardiovascular disease [15]. Although there is insufficient evidence to suggest that lifestyle changes will affect the outcome of the pregnancy, there is well-established long-term data showing that lifestyle changes can significantly reduce the likelihood of target organ damage. Pregnant women are often motivated to make behavior changes, and with the frequency of prenatal visits, pregnancy provides an opportunity to provide important education about healthy lifestyles.

The initial lab evaluation for a nonpregnant woman with new hypertension should include CBC, creatinine, electrolytes, urinalysis, TSH, calcium, EKG, and fasting blood sugar and fasting lipids. In pregnancy, the lipid panel may be deferred until 12 weeks postpartum as lipid levels may be affected by pregnancy, and an appropriate screening test for diabetes in pregnancy should be done rather than the fasting blood sugar. Otherwise, this evaluation should be completed for all women with a new diagnosis of hypertension, whether pregnant or not. Many clinicians also find it helpful to document baseline preeclampsia labs in women at risk of preeclampsia.

A careful review of both maternal and fetal risks and benefits must be considered in the decision to use pharmacologic therapy in the treatment of hypertensive disorders of pregnancy. In women with systolic blood pressure >160 or diastolic blood pressure >110, there is good evidence that medications should be initiated to prevent acute maternal end-organ damage, particularly stroke [16]. However, the benefit of antihypertensive therapy in mild to moderate hypertension (SBP 140–159 or DBP 90–109) has not been demonstrated in clinical trials. A 2007 meta-analysis showed a 50 % reduction in the risk of severe hypertension, but no reduction in preeclampsia, perinatal mortality, preterm birth, or SGA infant [17]. In fact aggressive lowering of blood pressure in pregnancy may be associated with harm. A 2002 study found that treatment of mild to moderate hypertension in pregnancy was associated with a significant reduction in birth weight. This effect was consistent regardless of etiology of hypertension or choice of medication [18]. International guidelines differ with respect to threshold for starting antihypertensive medications and blood pressure goals in the management of hypertension in pregnancy, but most agree that mild to moderate hypertension over the course of 9 months of pregnancy is unlikely to result in significant poor maternal or fetal outcomes [19–23].

Therefore, women with SBP < 160 ANDDBP < 110 mmHg are candidates for non-pharmacologic management and should not be started on medications.

It is best to discuss plans for management of chronic hypertension before conception. Since 50 % of pregnancies are unplanned, women in their reproductive years are best treated with a medication whose safety in pregnancy has been established. For women with chronic hypertension, it is likely that blood pressure will drop in the first half of gestation due to physiologic vasodilation. In women with no target organ damage, it is reasonable to discontinue antihypertensive therapy in early gestation and monitor closely for rising BP. Medication should be restarted if BP rises >160/100.

There are no large, randomized controlled trials to help guide decisions about which antihypertensive medication to use in pregnant women. Head-to-head comparisons on specific medications are limited, and well-designed trials evaluating pregnancy outcome and fetal safety are inadequate. Drugs of first choice in pregnancy are those with an acceptable safety profile and include labetalol and methyldopa. Methyldopa has been used extensively in pregnancy and long-term safety has been demonstrated [24]. However, its side effect profile often limits dosing that is adequate to achieve blood pressure control. Labetalol is a nonselective beta-blocker with vascular alpha-blocking properties and has been postulated to preserve uteroplacental blood flow better than other beta-blockers. It has been found to be both safe and effective [25–28] with fewer side effects than methyldopa and has become the first choice for treatment of hypertension in pregnancy.

Alternative beta-blockers include pindolol and metoprolol. Other beta-blockers, especially propranolol and atenolol, are best avoided due to individual reports of adverse outcomes such as preterm labor, neonatal bradycardia, and fetal growth restriction [29]. Calcium channel blockers are considered a second-line drug for hypertension in pregnancy. Nifedipine is the most widely used calcium channel blocker in pregnancy and is not associated with teratogenic risk [30]. Data on efficacy and long-term safety are limited. Amlodipine, used widely in the nonpregnant population, has not been studied in pregnancy and is best avoided. Hydralazine is most commonly used as an intravenous treatment of acute severe hypertension in the setting of preeclampsia. A meta-analysis demonstrated a slightly increased rate of adverse events with hydralazine compared to labetalol, but the evidence was not sufficient to make a definitive recommendation for one drug over the other [31]. The use of thiazide diuretics in pregnancy is controversial. Blood volume in pregnancy increases by 50 %, and while studies have not shown an association between diuretic use and adverse pregnancy outcomes [3], there are data demonstrating that diuretic use counteracts this normal expansion of blood volume.

ACE inhibitor use in the first trimester is associated with an increased risk of congenital abnormalities [32]. In addition, fetal renal abnormalities have been reported with ACE inhibitor use in the latter half of pregnancy. ARBs, direct renin inhibitors, while not studied in pregnancy, have a similar mechanism of action, so may pose similar risk. These drugs are contraindicated in pregnant women and should be discontinued in women planning pregnancy [32]. Table 8.4 presents a summary of antihypertensive medications in pregnancy.