Cardiovascular changes related to normal pregnancy begin early, prior to full placentation (Guedes-Martins et al. 2014, 2015a, b). Those changes include an increase in cardiac output, blood volume expansion, peripheral vasodilation and blood pressure reduction.

As in normotensive gestations (Strevens et al. 2001; Gaillard et al. 2011), in chronic hypertensive pregnant women the shapes of BP trajectories are characterized by a decrease until mid-pregnancy followed by an increase late in pregnancy, when it rises to return to prepregnancy values (Guedes-Martins et al. 2015c). This BP decrease begins early in the first trimester, and the physiological decrease in blood pressure, approximately 10 mmHg, is noted until the third trimester, at which time the BP profile tends to return to the patient’s standard (typical of the non-pregnant state).

As a result, some hypertensive women become normotensive during pregnancy, which can delay the diagnosis of disease or confuse it with the occurrence of a hypertensive condition related to pregnancy itself (e.g., preeclampsia, gestational hypertension). Consequently, in such cases the diagnosis of chronic hypertension can only be performed after 12 weeks postpartum if the blood pressure values are not normalized (The American College of Obstetricians and Gynecologists 2013).

Chronic hypertension is a disease that can be well tolerated during pregnancy, and in some cases, cHT pregnancies have a normal outcome without maternal and fetal complications. However, specialized attention should be given to these pregnant women because cHT is an established risk factor for poor obstetrical outcomes.

Adverse outcomes are particularly observed in women with cHT with uncontrolled severe hypertension, in those with target organ damage, and in those who are noncompliant with prenatal visits. In addition, adverse outcomes are substantially increased in women who develop superimposed preeclampsia, which complicates 17–25 % of cHT pregnancies (vs. a 3–5 % preeclampsia frequency described for the general population) (Sibai 2002).

Superimposed preeclampsia is the most prevalent complication in pregnant women with chronic hypertension. Chappel and colleagues (2008) presented prospective contemporaneous data on the outcome of pregnancies in women with chronic hypertension. In their study (Chappell et al. 2008), indices of maternal and perinatal morbidity and mortality were determined using prospectively collected data for 822 women with chronic hypertension. The incidence of superimposed preeclampsia was 22 % with early onset preeclampsia (≤34 weeks gestation) accounting for nearly half (44 %) of these cases (Chappell et al. 2008). Delivering an infant <10th customized birthweight percentile complicated 48 % (87/180) of those with superimposed preeclampsia and 21 % (137/642) of those without (relative risk [RR] 2.30; 95 % confidence intervals [CI_95%] 1.85–2.84) (Chappell et al. 2008). Delivery at <37 weeks gestation occurred in 51 % of those with superimposed preeclampsia (98 % of these iatrogenic) and 15 % of those without (66 % iatrogenic) (RR 3.52; 95 % CI_95% 2.79–4.45) (Chappell et al. 2008). The results obtained by Chappell and colleagues suggests that the prevalence of infants born small for gestational age and preterm is considerably higher than background rates and is increased further in women with superimposed preeclampsia (Chappell et al. 2008). The results were similar to that reported by three previous, robust, observational studies of women with chronic hypertension (Rey and Couturier 1994; McCowan et al. 1996; Sibai et al. 1998). Nevertheless, even without superimposed preeclampsia, women with cHT have significantly higher frequencies of perinatal death and small-for-gestational-age newborns than do normotensive women (Rey and Couturier 1994).

As a corollary, an extensive systematic review reporting meta-analyzed data from 55 studies of approximately 800,000 pregnancies (Bramham et al. 2014) showed that adverse outcomes of cHT pregnancy are common, and that review emphasized a need for adequate antenatal surveillance (Table 2).

Bramham and colleagues (2014) reported that women with chronic hypertension had high pooled incidences of superimposed pre-eclampsia (25.9 %, CI_95% 21.0–31.5 %), caesarean delivery (41.4 %, CI_95% 35.5–47.7 %), preterm delivery <37 weeks gestation (28.1 % CI_95% 22.6–34.4 %), birth weight <2500 g (16.9 %, CI_95% 13.1–21.5 %), neonatal intensive care unit admission (20.5 %, CI_95% 15.7–26.4 %), and perinatal death (4.0 %, CI_95% 2.9–5.4 %). In their systematic review, the incidences of adverse outcomes showed significantly higher risks in those with cHT: the relative risks were 7.7 (CI_95% 5.7–10.1) for superimposed pre-eclampsia compared with pre-eclampsia, 1.3 (CI_95% 1.1–1.5) for caesarean delivery, 2.7 (CI_95% 1.9–3.6) for preterm delivery <37 weeks gestation, 2.7 (CI_95% 1.9–3.8) for birth weight <2500 g, 3.2 (CI_95% 2.2–4.4) for neonatal intensive care unit admission, and 4.2 (CI_95% 2.7–6.5) for perinatal death (Bramham et al. 2014). These results should guide counseling, adequate drug treatment, and pre-pregnancy optimization of women affected by cHT (The American College of Obstetricians and Gynecologists 2013; Bramham et al. 2014).

The American College of Obstetricians and Gynecologists (2013) recommends preconception explanation of the risks associated with chronic hypertension and education about the signs and symptoms of preeclampsia. The presence of diabetes, obesity, kidney disease, history of early preeclampsia, uncontrolled hypertension, and secondary hypertension are considered risk factors for the development of superimposed preeclampsia (The American College of Obstetricians and Gynecologists 2013). However, some evidence suggests that in women with chronic hypertension, a history of preeclampsia does not increase the rate of superimposed preeclampsia, but is associated with an increased rate of delivery at <37 weeks (Sibai et al. 2011). The ACOG and the National Institute for Health and Care Excellence guidelines guidance (2015) also recommends pre-conception discontinuation of medications with known fetal adverse effects, in particular angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers, mineralocorticoid antagonists, and statins.

The Report of the National High Blood Pressure Education Program Working Group on High Blood Pressure in Pregnancy advises for the assessment for ventricular hypertrophy, retinopathy and renal disease in women with history of hypertension for more than several years because target organ damage, especially renal disease, can progress during pregnancy (Report of the National High Blood Pressure Education Program Working Group on High Blood Pressure in Pregnancy 2000). In women with severe hypertension of long duration (more than 4 years), assessment of left ventricular function with echocardiography or electrocardiography is considered good clinical practice (The American College of Obstetricians and Gynecologists 2013). This recommendation is also enhanced by the Canadian (Magee et al. 2014), Australasian and JNC 8 evidence guidelines for the management of high blood pressure in adults (James et al. 2014), reinforcing the importance of looking for signs and symptoms of secondary hypertension in women with cHT who seek preconception counseling. Particularly, the presence of resistant hypertension, hypokalemia (potassium levels less than 3.0 mEq/L), elevated serum creatinine level (greater than 1.1 mg/dL) and family history of kidney disease are important suggestive findings of secondary hypertension. Additionally, if the urinalysis is positive for protein, then a 24-h urine collection for protein analysis or measurement of spot urine protein-to-creatinine ratio can be assessed (Côté et al. 2008). This analysis might assist in the diagnosis of superimposed preeclampsia and can provide prognostic information about the development of fetal growth restriction when prepregnancy proteinuria is found (Seely and Ecker 2014; Sibai et al. 1998). The baseline concentrations of serum creatinine, electrolytes, uric acid, liver enzymes, and platelet count should be documented before conception to use as comparators if superimposed preeclampsia is suspected (The American College of Obstetricians and Gynecologists 2013). The ACOG task force recommendation (The American College of Obstetricians and Gynecologists 2013) also suggests referral to a physician with expertise in treating hypertension if secondary hypertension is suspected.

For the general population with cHT, the use of home BP monitoring in daily clinical practice is a useful instrument as an aid to achieving targets and monitoring responses to medication (Maldonado et al. 2009). For pregnant women with chronic hypertension and poorly controlled BP, the use of home BP monitoring is suggested, particularly in the second half of pregnancy when most superimposed preeclampsia occurs (The American College of Obstetricians and Gynecologists 2013). In particular, ambulatory BP monitoring can be of special interest for women with suspected white coat hypertension, avoiding overtreatment of BP and unnecessary adverse effects of treatment when not indicated (The American College of Obstetricians and Gynecologists 2013; James et al. 2014).

Mild to moderate hypertension during pregnancy is a common finding. In daily clinical practice, antihypertensive drugs are often used in the belief that lowering blood pressure will prevent progression to more severe disease and thereby improve the outcome, reducing maternal morbidity by limiting episodes of severe hypertension (Seely and Ecker 2014; Abalos et al. 2014). However, it remains unclear whether antihypertensive drug therapy for mild to moderate hypertension during pregnancy is worthwhile (Abalos et al. 2014). In addition, overly aggressive antihypertensive treatment might decrease fetoplacental perfusion, increase the risk of fetal growth restriction (Seely and Ecker 2014; von Dadelszen et al. 2000), and reproduce fetal effects of diseases related to placental bed dysfunction.

Recently, the Control of Hypertension in Pregnancy Study (CHIPS) was designed to compare tight control (the use of antihypertensive therapy to normalize BP) with less-tight control of non-proteinuric, non-severe hypertension in pregnancy with respect to perinatal and maternal outcomes (Magee et al. 2015). CHIPS was an open, international, randomized, multicenter trial involving 987 women. The primary outcome was a composite of pregnancy loss (defined as miscarriage, ectopic pregnancy, pregnancy termination, stillbirth, or neonatal death) or high-level neonatal care (defined as greater-than-normal newborn care) for more than 48 h until 28 days of life or until discharge home, whichever was later. The secondary outcome was serious maternal complications occurring up to 6 weeks postpartum or until hospital discharge, whichever was later (Martin et al. 2005). This randomized trial showed that less-tight control of maternal hypertension in pregnancy compared with tight control resulted in no significant difference in the risk of adverse perinatal outcomes, as assessed by the rates of perinatal death or high-level neonatal care for more than 48 h (primary outcome) (Brown et al. 2000). Additionally, less-tight (vs. tight) control did not significantly increase the risk of overall serious maternal complications (secondary outcome). However, with respect to the mothers, the CHIPS findings are consistent with a meta-analysis of previous trials that showed that less-tight versus tight control increases the incidence of severe maternal hypertension (but not preeclampsia) (Abalos et al. 2014; Magee et al. 2015), which is considered a risk factor for acute stroke during and outside of pregnancy (James et al. 2014; Martin et al. 2005). The treatment of severe hypertension (systolic BP more than 160 mmHg and/or diastolic BP more than 110 mmHg) is always recommended because it is believed to reduce the risk of maternal stroke and coronary events and to limit episodes of severe hypertension. However, the exact goal ranges for BP targets during pregnancy in women with chronic hypertension are not established.

The ACOG recommends antihypertensive therapy for pregnant women with persistent chronic hypertension with systolic BP of 160 mmHg or higher or diastolic BP of 105 mmHg or higher (The American College of Obstetricians and Gynecologists 2013). For pregnant women with chronic hypertension treated with antihypertensive medication, the ACOG suggests that BP levels be maintained between 120 mmHg systolic and 80 mmHg diastolic, and 160 mmHg systolic and 105 mmHg diastolic. The NHBPEP (Report of the National High Blood Pressure Education Program Working Group on High Blood Pressure in Pregnancy 2000) working group considers tapering antihypertensive medications and reinstituting or increasing the dose of antihypertensive drugs if BP is >150–160 mmHg systolic or >100–110 mmHg diastolic. Additionally, the JNC-8 suggests continuing medication if there is target-organ damage or a previous requirement for multiple antihypertensive agents for BP control, and if medication is stopped, instituting pharmacological treatment if BP is >150–160 mmHg systolic or >100–110 mmHg diastolic (James et al. 2014). The Society of Obstetricians and Gynaecologists of Canada (Magee et al. 2014) recommends treatment if BP is >159 mmHg systolic or >109 mmHg diastolic to reduce maternal risk with a target of <156 mmHg systolic and <106 mmHg diastolic in patients without cardiovascular risk factors. Finally, the Australasian Society for the Study of Hypertension in Pregnancy (Brown et al. 2000) suggests antihypertensive therapy in cases of BP >170 mmHg systolic or >110 mmHg diastolic with a recommended target of 120–140 mmHg systolic and 80–90 mmHg diastolic.

For women who enter pregnancy and receive antihypertensive therapy prior to conception, there are scarce or absent data to guide decisions regarding continuing or discontinuing therapy (The American College of Obstetricians and Gynecologists 2013).

The more commonly used antihypertensive agents with an acceptable safety profile in pregnancy and their Food and Drug Administration (FDA) classification are illustrated in Table 3.