Chronic hypertension in pregnancy: Prenatal and postpartum care

INTRODUCTION — In pregnant patients, chronic hypertension (also called preexisting hypertension) can be defined as hypertension known to be present before conception or first recognized before 20 weeks of gestation. In patients with a previous pregnancy complicated by gestational hypertension, hypertension that persists 12 or more weeks after giving birth is also classified as chronic.

Patients with chronic hypertension are at risk for a variety of adverse maternal and fetal/neonatal outcomes (table 1), some of which can be mitigated by appropriate pregnancy management.

This topic will discuss the risks and management of pregnancy complicated by chronic hypertension. Treatment of high blood pressure in pregnancy is reviewed separately. (See "Treatment of hypertension in pregnant and postpartum patients".)

DEFINITION/DIAGNOSTIC CRITERIA

Pregnancy — Diagnostic definitions for the various hypertensive disorders associated with pregnancy are described in the table (table 2) [1,2].

Blood pressure criteria for hypertension in pregnancy are [3]:

●Hypertension – Systolic blood pressure ≥140 mmHg, diastolic blood pressure ≥90 mmHg, or both.

●Severe hypertension – Systolic blood pressure ≥160 mmHg, diastolic blood pressure ≥110 mmHg, or both.

Hypertension should be confirmed by at least two measurements (at least four hours apart except for blood pressures in the severe range, which should be repeated sooner and treated).

In pregnant patients who first present for prenatal care in the second trimester without recent prepregnancy blood pressure measurements for comparison, the diagnosis of chronic hypertension can be missed due to the normal physiologic decrease in blood pressure between 12 and 19 weeks of gestation: systolic and diastolic blood pressures are approximately 5 to 10 mmHg below baseline at this time. (See "Maternal adaptations to pregnancy: Cardiovascular and hemodynamic changes", section on 'Changes in systemic hemodynamics'.)

Nonpregnant individuals — Blood pressure criteria for hypertension had been the same in pregnant and nonpregnant individuals until 2017, when the American College of Cardiology (ACC) and the American Heart Association (AHA) modified the traditional criteria for diagnosing hypertension in nonpregnant adults to better identify and modify long-term cardiovascular risk [4] (see "Overview of hypertension in adults", section on 'Definitions'). Under the new criteria, blood pressure criteria for hypertension in nonpregnant adults are [5]:

●Elevated blood pressure – Systolic blood pressure 120 to 129 mmHg and diastolic blood pressure <80 mmHg.

●Stage 1 hypertension – Systolic blood pressure 130 to 139 mmHg or diastolic blood pressure 80 to 89 mmHg.

●Stage 2 hypertension – Systolic blood pressure ≥140 mmHg or diastolic blood pressure ≥90 mmHg.

These new criteria are estimated to at least double the number of reproductive-age females in the United States diagnosed with chronic hypertension [4,6,7], but the pregnancy implications remain unclear. A meta-analysis demonstrated a stepwise relationship between the ACC/AHA blood pressure categories above and the strength of the association with preeclampsia [8]. There was a progressive increase in risk ratios (RRs) from the elevated blood pressure category (RR 2.0, 95% prediction interval [PI] 0.8-4.8) to stage 1 hypertension (RR 3.0, 95% PI 1.1-8.5) to stage 2 hypertension (RR 7.9, 95% PI 1.8-35.1). However, the authors concluded that lowering the blood pressure threshold below 140/90 mmHg at <20 weeks of gestation would not assist clinicians in identifying patients at heightened maternal or perinatal risk since the negative likelihood ratio was >2.0.

In this topic, the term "chronic hypertension" will be used to refer to patients who meet current ACC/AHA criteria for stage 2 hypertension unless otherwise noted. Further evidence is needed to determine whether pregnancy management should differ for those with stage 1 versus stage 2 hypertension. The American College of Obstetricians and Gynecologists suggests a conservative management approach to patients with stage 1 hypertension, such as closer maternal monitoring during pregnancy [2]

EPIDEMIOLOGY — Among pregnant individuals in the United States, the prevalence of chronic hypertension was 2.3 percent in 2019 [9]. The prevalence has increased severalfold in recent decades, largely related to increasing maternal age and increasing obesity in the population. The prevalence is twofold higher in pregnant Black individuals compared with pregnant White individuals (4.3 versus 2 percent). (See "Overweight and obesity in adults: Health consequences", section on 'Hypertension' and "Overweight, obesity, and weight reduction in hypertension".)

RISKS OF CHRONIC HYPERTENSION IN PREGNANCY — Chronic hypertension and cardiovascular disease are among the leading causes of maternal and fetal/neonatal morbidity and mortality (table 1) [10,11]. Superimposed preeclampsia, which develops in 13 to 40 percent of pregnant individuals with chronic hypertension, increases the risk of adverse outcomes [12,13]. (See 'Patients with superimposed preeclampsia' below.)

The frequency of adverse outcomes is difficult to cite precisely because reports do not uniformly distinguish between pregnancies complicated by superimposed preeclampsia and those with uncomplicated chronic hypertension alone. Where possible, we will review outcomes of patients with chronic hypertension alone, acknowledging that most analyses combine these outcomes with those in patients with superimposed preeclampsia.

Maternal risks — Population-based studies, as well as systematic reviews and meta-analyses, consistently demonstrate an increased risk of adverse maternal outcomes associated with chronic hypertension in pregnancy [10,14-18]. The risk increases with the severity of hypertension and presence of end-organ damage [19-22]. Although the relative risks (RR) for these complications are significantly increased, the absolute risk for serious end-organ damage (eg, heart, kidney, brain) is low in the absence of preeclampsia or uncontrolled hypertension. Obesity may be a confounder since it is associated with hypertension, diabetes, insulin resistance, chronic inflammation, and endothelial dysfunction [23].

●Acute kidney failure – 5.9 per 1000 deliveries (odds ratio [OR] 14.6, 95% CI 12.1-17.7) [10].

●Pulmonary edema – 1.5 per 1000 deliveries (OR 9.3, 95% CI 6.7-12.9) [10].

●Superimposed preeclampsia – 13 to 40 percent [10,12,13,24] (RR 7.7, 95% CI 5.7-10.1) [25].

●In-hospital mortality – 0.4 per 1000 deliveries (OR 6.2, 95% CI 3.3-11.5) [10].

●Stroke/cerebrovascular complications – 2.7 per 1000 deliveries (OR 5.4, 95% CI 4.3-6.9) [10].

●Cesarean birth – Estimated prevalence 41.4 percent (95% CI 35.5-47.7) [16] (OR 2.7, 95% CI 2.4-3) [15].

●Placental abruption (adjusted OR 2.3, 95% CI 1.5-3.5) [18], with the highest risk in patients with superimposed preeclampsia [12,18,26].

●Postpartum hemorrhage (OR 2.2, 95% CI 1.4-3.7) [15].

●Gestational diabetes – 8.1 percent (adjusted OR 1.6, 95% CI 1.3-2.1) [15], likely reflecting common risk factors, such as obesity, and similar pathogenic mechanisms, such as insulin resistance [16,17,27].

●Hospitalization – Mean inpatient length of stay for chronic hypertension without preeclampsia 5.4 days (standard deviation [SD] 7 days) [24] and 12.7 days (SD 9.3) for superimposed preeclampsia; odds of length of stay >6 days (OR 6.7, 95% CI 6.2-7.3) [10,27].

Fetal/neonatal risks — Rates of adverse perinatal outcomes are higher among offspring of mothers with longer duration and greater severity of hypertension, presence of end-organ damage, and occurrence of superimposed preeclampsia.

●Perinatal mortality – Perinatal mortality is two to four times higher in pregnancies complicated by chronic hypertension compared with pregnancies in the general obstetric population, and the increase persists after adjusting for preeclampsia and birth weight [15,25,28,29]. The increase in perinatal mortality is likely attributable to increases in indicated preterm birth and fetal growth restriction (FGR).

●Preterm birth, low birth weight, neonatal intensive care unit admission – In a meta-analysis comparing pregnancy outcomes of individuals with chronic hypertension with population-based data (55 studies, nearly 800,000 pregnancies), patients with chronic hypertension had a threefold increase in the pooled incidence of the following outcomes [25]:

•Preterm birth <37 weeks (33 and 12 percent, respectively, RR 2.7, 95% CI 1.9-3.6).

•Birth weight <2500 grams (22 and 8 percent, respectively, RR 2.7, 95% CI 1.9-3.8).

•Newborns admitted to the neonatal intensive care unit (19 and 6 percent, respectively, RR 3.2, 95% CI 2.2-4.4).

●Small for gestational age – In a prospective cohort study of pregnant patients receiving care in the United Kingdom that compared outcomes of those with chronic hypertension (n = 1417) to those without (n = 108,515), patients with chronic hypertension were twice as likely to give birth to a small for gestational age (SGA) newborn (19.2 versus 10.9 percent, adjusted OR 2.06, 95% CI 1.79-2.39) [15]. The increased risk of SGA with chronic hypertension was not confined to patients with superimposed preeclampsia; in stratified analysis of those with chronic hypertension alone, the odds of an SGA neonate remained elevated (OR 1.66, 95% CI 1.41-1.95). Other reports indicate even higher rates of SGA for patients with chronic hypertension, exceeding 30 percent [30,31].

●Congenital malformations – In both untreated and treated patients with chronic hypertension, chronic hypertension in pregnancy has also been associated with an increased risk for congenital malformations, with RR estimates for congenital cardiac malformations ranging from 1.4 to 1.5 for untreated hypertension and 1.6 to 2 for treated hypertension [32,33]. Smaller studies have suggested an increase in other anomalies, including esophageal atresia and hypospadias [34]. Further investigation is needed to understand the pathophysiology underlying these associations. We believe these findings warrant obtaining a fetal anatomic survey at 18 to 20 weeks of gestation (which is routine even in patients without chronic hypertension), but not routine fetal echocardiography, which should be ordered selectively for standard indications. (See "Congenital heart disease: Prenatal screening, diagnosis, and management".)

Long-term prognosis

●Maternal – Both chronic hypertension and preeclampsia are clearly associated with increased cardiovascular risk in later life [35-39]. (See "Overview of hypertension in adults", section on 'Complications of hypertension' and "Overview of atherosclerotic cardiovascular risk factors in females", section on 'Hypertensive disorder of pregnancy' and "Preeclampsia: Intrapartum and postpartum management and long-term prognosis", section on 'Long-term maternal risks of pregnancy-associated hypertension'.)

●Offspring – The existing data on long-term offspring outcomes of pregnancies complicated by chronic hypertension are largely population-based and do not always account for preeclampsia, medication use, severity of disease, and gestational age at birth. With these limitations, long-term follow-up of offspring of pregnancies complicated by hypertensive disorders in the Helsinki Birth Cohort showed a modest association with self-reported cognitive decline and mental and mood disorders [40-42]. Kidney, immune, endocrine, and gastrointestinal system abnormalities in children and adolescents have also been associated with in utero exposure to hypertensive disorders in pregnancy [43].

PRECONCEPTION CARE — Ideally, patients with chronic hypertension are seen prior to conception to address the following issues, which are summarized in the table (table 3), in addition to routine preconception assessments (see "The preconception office visit"). Maternal-fetal medicine consultation should be considered for counseling and management both preconception and during pregnancy.

●Counseling – Counseling is provided about the pregnancy risks of chronic hypertension and the potential interventions to minimize these risks. Patients are informed about the anticipated course of pregnancy, need for heightened maternal and fetal surveillance, and likely need for more frequent obstetric visits and possibly hospitalization (eg, if superimposed preeclampsia develops) compared with a low-risk population. (See 'Risks of chronic hypertension in pregnancy' above and 'Patients with superimposed preeclampsia' below.)

●Consideration of secondary causes of hypertension – While the majority of hypertensive, reproductive-age females with chronic hypertension have essential (idiopathic or primary) hypertension, consideration of secondary causes of hypertension is important (summarized in the table (table 4)), if not already evaluated, since these causes can require specific testing and therapy, ideally before pregnancy. A finding suggestive of secondary hypertension is resistant hypertension, particularly in younger patients (<30 years) with no family history of hypertension. (See "Initial evaluation of adults with hypertension" and "Evaluation of secondary hypertension".)

●Laboratory tests

•Creatinine

•Urine protein/creatinine ratio or 24-hour urine protein

If abnormal, detailed information on issues related to chronic kidney disease in pregnancy is available separately. (See "Pregnancy and contraception in patients with nondialysis chronic kidney disease".)

●Cardiac evaluation – Baseline cardiac evaluation is recommended in patients with long-standing hypertension, based on age or poorly controlled hypertension for more than four years, given the increased risk of cardiac hypertrophy, dysfunction, and ischemic heart disease [2]. Because of the enhanced detection of left ventricular hypertrophy and cardiac dysfunction, we utilize transthoracic echocardiography for baseline cardiac evaluation. When echocardiography is not available, a twelve-lead electrocardiogram can be used as an alternative first-line test. (See "Initial evaluation of adults with hypertension".)

Issues related to pregnant patients with acquired heart disease are discussed in detail separately. (See "Acquired heart disease and pregnancy".)

●Blood pressure management – For patients who have achieved stable blood pressure control with pharmacotherapy and are considering pregnancy or attempting to conceive, the risks and benefits of continuing a stable antihypertensive drug regimen versus changing the regimen to the few drugs preferred for use in pregnant patients (labetalol, nifedipine, methyldopa) must be considered. For patients who have not achieved stable blood pressure control, blood pressure should be optimized. We suggest shared decision-making involving the obstetrician/maternal-fetal medicine specialist, primary care provider, and patient. Drug choice and target blood pressure are discussed in detail separately. (See "Treatment of hypertension in pregnant and postpartum patients", section on 'Preconception management of chronic hypertension'.)

However, angiotensin converting enzyme inhibitors and angiotensin receptor blockers should be discontinued before pregnancy since they have been associated with congenital malformations, including renal dysgenesis and calvarial hypoplasia, as well as fetal growth restriction and oligohydramnios [44-46]. (See "Adverse effects of angiotensin converting enzyme inhibitors and receptor blockers in pregnancy", section on 'Clinical approach to use of RAAS inhibitors in females of childbearing potential'.)

●Modifiable risk factors – Weight loss in patients who are overweight or obese, smoking cessation in smokers, increased exercise for sedentary individuals, and dietary changes (eg, sodium restriction, Dietary Approaches to Stop Hypertension [DASH] diet) when appropriate are encouraged as nonpharmacologic means of reducing blood pressure and potentially improving pregnancy outcome and overall health. (See "Overview of hypertension in adults", section on 'Nonpharmacologic therapy' and "Exercise during pregnancy and the postpartum period" and "Obesity in pregnancy: Complications and maternal management" and "Tobacco and nicotine use in pregnancy: Cessation strategies and treatment options".)

PRENATAL CARE AND DELIVERY

Patients with chronic hypertension — The following discussion applies to the prenatal care and delivery of patients with chronic hypertension without superimposed preeclampsia. Monitoring for development of superimposed preeclampsia is a key component of the prenatal care of these patients. If it develops, pregnancy management needs to be modified because preeclampsia is a progressive and potentially life-threatening disease. (See 'Patients with superimposed preeclampsia' below.)

Baseline clinical evaluation, laboratory testing, and preeclampsia prophylaxis

●Clinical evaluation should include baseline blood pressure and heart rate and a general physical examination, including cardiopulmonary auscultation and evaluation for any signs of cardiac dysfunction (ie, cyanosis, hepatomegaly, jugular venous distention, pulmonary edema).

●In addition to routine prenatal laboratory testing, the following laboratory tests are recommended, if not obtained within the six months prior to conception:

•Creatinine

•Urine protein/creatinine ratio or 24-hour urine protein

We also obtain liver transaminases (aspartate aminotransferase and alanine aminotransferase) and a platelet count as a baseline, as this information is useful if the patient develops signs/symptoms of preeclampsia later in pregnancy. We obtain electrolytes in patients with kidney dysfunction. We test for overt diabetes in patients with obesity. (See "Gestational diabetes mellitus: Screening, diagnosis, and prevention", section on 'Screening for overt diabetes in early pregnancy'.)

●If not assessed within one year prior to conception, transthoracic echocardiography or a twelve-lead electrocardiogram is suggested for patients with long-standing hypertension, based on age or poorly controlled hypertension for more than four years [2]. Cardiac dysfunction increases morbidity in pregnancy and peripartum, given the increase in cardiac output and cardiac stress. (See 'Preconception care' above.)

●Accurate gestational dating is particularly important given the increased risks for growth restriction and indicated preterm birth in patients with chronic hypertension. Whether to perform a dating ultrasound examination in the first trimester or wait until the time of the 18- to 20-week fetal anatomic survey depends on the clinician's confidence in the menstrual dates. (See "Prenatal assessment of gestational age, date of delivery, and fetal weight".)

●Low-dose aspirin is recommended after 12 weeks of gestation for preeclampsia prophylaxis as these patients are at high risk of developing the disease [47]. Based on the existing evidence and dose availability in the United States, we use 81 mg daily. Some have advocated higher doses (100 to 150 mg daily) based on a meta-analysis of eight trials [48]; however, there was significant heterogeneity and none of the trials directly compared the higher doses with 81 mg.

Although the efficacy of low-dose aspirin has been established in meta-analyses of randomized trials of patients at high-risk of developing preeclampsia (see "Preeclampsia: Prevention", section on 'Evidence of efficacy'), a meta-analysis limited to patients with chronic hypertension did not show statistically significant reductions in superimposed preeclampsia (24.6 versus 30.0 percent; OR 0.74, 95% CI 0.47-1.16; four trials, 992 patients), SGA births, or perinatal mortality [49]. There was low certainty of this finding given the high risk of bias in the trials, inconsistency (aspirin was effective in two of the four trials), and high heterogeneity. Preterm birth was reduced (OR 0.63, 95% CI 0.45-0.89) based on moderate quality evidence. We use aspirin prophylaxis in patients with chronic hypertension given that evidence for lack of preeclampsia benefit and other outcomes is low quality and evidence for reduction of preterm birth is moderate quality.

●Initiation and discontinuation of antihypertensive therapy, as appropriate, which is discussed below. (See 'Blood pressure management' below.)

Diet and gestational weight gain — Patients should be encouraged to meet gestational weight gain targets that are appropriate for their body mass index (table 5). In particular, excessive gestational weight gain should be avoided because increased adiposity is strongly associated with higher blood pressure. Excessive gestational weight gain can also lead to significant postpartum weight retention. (See "Gestational weight gain", section on 'Recommendations for gestational weight gain'.)

There is minimal information on the effects of initiating a low salt or Dietary Approaches to Stop Hypertension (DASH) diet before pregnancy or continuing it throughout pregnancy [50-53]. However, these are healthy dietary approaches and would be reasonable to continue during pregnancy. (See "Treatment of hypertension in pregnant and postpartum patients", section on 'Diet'.)

Ongoing maternal monitoring — Obstetric provider visits should include measurement of blood pressure and assessment for potential symptoms of superimposed preeclampsia. More frequent visits than standard schedules (which may be at two- to four-week intervals) for blood pressure monitoring may be needed in the setting of poorly controlled blood pressure or if ongoing medication titration is needed.

●Blood pressures should be measured with the appropriate sized cuff, proper positioning, and after a five-minute rest period; ideally, a blood pressure cuff that has been validated in pregnancy should be used [54,55]. Home blood pressure monitoring is generally reliable, useful for complementing office visits, and may reduce office visits and the need for hospitalization [56,57]. We use this approach in our practice. In a meta-analysis, systolic blood pressure values measured at home were lower than office values by 4 mmHg (95% CI -6 to -3) and diastolic measurements were lower by 3 mmHg (95% CI -4 to -2) [58]. (See "Treatment of hypertension in pregnant and postpartum patients", section on 'Technique for accurate measurement of blood pressure'.)

While increasing blood pressure, possibly in the late second trimester and more commonly in the third trimester, could indicate the anticipated physiologic rise in blood pressure in the second half of pregnancy, superimposed preeclampsia must be excluded, based on gestational age at onset, symptoms and laboratory studies, risk factors, and course over time. We have a low threshold for in-hospital evaluation if superimposed preeclampsia is suspected. (See 'Clinical presentation and evaluation' below.)

●Patient education on the symptoms and signs of preeclampsia and clear instructions about when to contact providers are essential. Symptoms of persistent and/or severe headache, visual changes (scotomata, photophobia, blurred vision, or temporary blindness [rare]), right upper quadrant or epigastric pain, new onset of nausea or vomiting in the third trimester, new onset of shortness of breath, altered mental status, or vaginal bleeding warrant additional investigation. (See "Preeclampsia: Clinical features and diagnosis", section on 'Clinical presentation'.)

Blood pressure management — Recommendations for management of severe hypertension and nonsevere chronic hypertension in pregnancy are reviewed below, along with supporting evidence.

Although the American College of Cardiology and the American Heart Association have published recommendations for management of chronic hypertension in nonpregnant individuals, these guidelines are not fully generalizable to pregnant individuals due to fetal safety concerns and the physiologic changes of pregnancy and because the long-term goals of adult hypertension treatment over the course of a lifetime are different from those of the short-term time frame of pregnancy.

Severe hypertension — Regardless of etiology (chronic hypertension, gestational hypertension, preeclampsia), there is consensus among medical organizations that severe maternal hypertension (systolic blood pressure ≥160 mmHg or diastolic blood pressure ≥110 mmHg) should be pharmacologically treated in a timely manner to reduce the risk for maternal cerebrovascular, cardiac, and renal events, as well as death [2,59,60]. Evidence for this recommendation is extrapolated from studies on the management of preeclampsia and on management of severe hypertension in nonpregnant adults, with few studies conducted exclusively in pregnant patients with chronic hypertension [4,5,61]. (See "Preeclampsia with severe features: Delaying delivery in pregnancies remote from term", section on 'Morbidity and mortality' and "Management of severe asymptomatic hypertension (hypertensive urgencies) in adults" and "Evaluation and treatment of hypertensive emergencies in adults".)

The general principle is to gradually lower blood pressure below the severely elevated range and into the mildly elevated range, thereby avoiding an acute reduction in uterine artery blood flow. The optimal blood pressure target for maintenance therapy after this initial reduction is less clear. We believe a target blood pressure range of 120 to 139/80 to 89 mmHg is reasonable. (See "Treatment of hypertension in pregnant and postpartum patients", section on 'Oral maintenance therapy'.)

The choice of medication is based on need for acute versus chronic treatment of blood pressures as well as safety. Medications used for acute lowering of blood pressure in pregnancy include intravenous labetalol, intravenous hydralazine, or oral nifedipine (table 6). In a meta-analysis of 35 randomized trials involving 3573 pregnant patients comparing one antihypertensive agent against another, no agent was clearly superior [61]. Thus, the choice of antihypertensive agent should depend on availability, the clinician's experience and familiarity with a particular drug, and adverse effects.

Nonsevere hypertension

Patient subgroups

●Patients not on antihypertensive therapy and with no end-organ disease – For patients with chronic hypertension not on antihypertensive therapy and with no end-organ involvement, we recommend initiating treatment at blood pressure threshold of 140/90 mmHg using the fewest medications at the lowest effective dose to achieve this goal. Our approach is based on the benefits demonstrated in the Chronic Hypertension and Pregnancy (CHAP) trial [62] (See 'Evidence of potential benefits of treatment' below.)

A target blood pressure range of 120 to 139/80 to 89 mmHg after initiation of treatment is reasonable, although specific target blood pressure range was not fully addressed in the CHAP trial.

●Patients on antihypertensive therapy and with no end-organ disease – For patients with nonsevere hypertension on antihypertensive therapy with no end-organ involvement, our decision making is individualized. For most women with well-controlled blood pressures on an antihypertensive medication regimen with a good safety profile, it is reasonable to continue medications to decrease the occurrence of severe hypertension. A target blood pressure range of 120 to 139/80 to 89 mmHg is reasonable. However, it is also reasonable to discontinue medications during the first trimester to minimize fetal exposure and restart them if blood pressures meet the 140/90 mmHg threshold. With this approach, close blood pressure monitoring is imperative, and the blood pressure changes, such as the decline in the midtrimester and rise in the third trimester, must be considered. (See 'Choice of drug and dosing' below.)

●Patients with end-organ disease – For patients with nonsevere hypertension and end-organ involvement, such as heart or kidney disease, blood pressure management is paramount as uncontrolled hypertension may be associated with significant morbidity (see 'Choice of drug and dosing' below). After initiation of therapy, at a minimum, it is desirable to maintain blood pressure at 120 to 139/80 to 89 mmHg; whether lowering blood pressure to a "normal" level (ie, <120/80 mmHg) would confer maternal benefit is unresolved [20]. The American Diabetes Association suggests treating pregnant patients with diabetes and hypertension, with the blood pressure target of 110 to 135/85 mmHg to reduce the risk for accelerated maternal hypertension and minimize impaired fetal growth [63]. (See "Treatment of hypertension in patients with diabetes mellitus".)

The CHAP trial excluded patients with secondary hypertension or other significant comorbidities (eg, heart or kidney disease), thus the impact of antihypertensive therapy and optimal blood pressure target in these patients could not be evaluated [62].

Choice of drug and dosing — In patients with nonsevere hypertension, our preference is to start treatment with either labetalol, a long-acting calcium channel blocker (eg, extended-release nifedipine), or methyldopa (table 7). The dose is increased if at least two blood pressure measurements remain elevated. If maximum doses of one drug are ineffective to achieve the goal blood pressure range as discussed above, then a second or third drug can be added. It is important to closely monitor patients in whom blood pressure is not responding well to antihypertensive therapy since this may be a sign of preeclampsia. (See 'Clinical presentation and evaluation' below.)

Evidence of potential benefits of treatment

●In the 2022 open-label, multicenter, pragmatic Chronic Hypertension and Pregnancy (CHAP) trial, 2408 pregnant people <23 weeks of gestation with nonsevere chronic hypertension at 61 centers were randomly assigned to receive antihypertensive therapy at a threshold of 140/90 mmHg (active treatment) or no treatment until development of severe hypertension (defined as systolic BP≥160 or diastolic BP≥105 mmHg) (control group) [62]. Rates of the primary composite outcome (preeclampsia with severe features, medically indicated preterm birth at <35 weeks of gestation, abruption, or fetal or neonatal death) were reduced in the active treatment group (30.2 versus 37.0 percent; adjusted risk ratio [aRR] 0.82, 95% CI 0.74-0.92), with no significant difference in rates of fetal growth restriction or serious neonatal or maternal morbidity. This trial represents the most robust evidence to inform clinical practice.

●In a 2022 network meta-analysis of 72 randomized trials (pre-CHAP) including nearly 7000 participants addressing which antihypertensives are superior to placebo/no therapy or another antihypertensive drug for controlling nonsevere pregnancy hypertension, major findings were [64]:

•Commonly used antihypertensive drugs reduced the occurrence of severe hypertension by 30 to 70 percent compared with placebo/no treatment

•Labetalol reduced proteinuria/preeclampsia (odds ratio [OR] 0.73, 95% CI 0.54-0.99) and fetal/newborn death (OR 0.54, 95% CI 0.30-0.98) compared with placebo/no therapy

•Labetalol reduced proteinuria/preeclampsia compared with methyldopa (OR 0.66, 95% CI 0.44-0.99) and calcium channel blockers (OR 0.63, 95% CI 0.41–0.96).

No other differences were identified. The possible benefit of labetalol over other antihypertensive drugs should be interpreted with caution given the wide confidence intervals.

Beyond noted benefits reflected in trial data, prevention of severe hypertension in pregnant individuals with chronic hypertension may have additional benefits. Experts point out that the failure to identify and treat severe maternal hypertension has been recognized in reviews of maternal deaths as the single most important failure in the care of patients with pregnancy-associated hypertension [65].

Evidence of potential harms of treatment — The international multicenter randomized Control of Hypertension in Pregnancy (CHIPS) trial was designed to test the effects of less tight control (target diastolic blood pressure 100 mmHg) versus tight control (target diastolic blood pressure 85 mmHg) on pregnancy complications [65,66]. Most (75 percent) of the 987 participants in the trial had chronic hypertension. In a subgroup analysis of patients with chronic hypertension, less tight blood pressure control reduced the odds of small for gestational age (SGA) birth weight, with the upper confidence interval just missing statistical significance (aOR 0.66, 95% CI 0.44-1.00). However, key concerns have been raised with respect to extrapolating the results of CHIPS to patients with mild and moderate chronic hypertension. For example, the sample size of this subgroups of patients was inadequate to evaluate key perinatal outcomes such as SGA and indicated preterm birth. In addition, only a small percentage of patients with mild and moderate hypertension were enrolled prior to 20 weeks, and over one-half of the patients stayed on antihypertensive therapy at randomization, so there was inadequate comparison between antihypertensive therapy and no therapy.

In light of these concerns as well as newer data from the CHAP trial showing no increase in rates of fetal growth restriction with a 140/90 mmHg threshold for antihypertensive treatment in pregnant people with chronic hypertension, we believe that the association between tight control and SGA found in the subset of patients with chronic hypertension enrolled in CHIPS does not justify withholding antihypertensive treatment for blood pressures exceeding 140/90 mmHg.

Recommendations of selected medical organizations

●American College of Obstetricians and Gynecologists (ACOG) – ACOG has recommended utilizing 140/90 mmHg as the threshold for initiation or titration of medical therapy for chronic hypertension in pregnancy, rather than the previously recommended threshold of 160/110 mmHg [67]. ACOG has not made specific recommendations for patients with end-organ involvement.

●National Institute for Health and Care Excellence (NICE) – NICE guidelines recommend offering treatment for systolic blood pressure ≥140 mmHg or diastolic blood pressure ≥90 mmHg, with goal blood pressures of <135/85 mmHg [60].

●International Society for the Study of Hypertension in Pregnancy (ISSHP) – The ISSHP recommends pharmacologic therapy to keep blood pressures in the range of 110 to 140 mmHg/80 to 85 mmHg during pregnancy [59].

Screening for fetal growth restriction — Our general approach to screening for fetal growth restriction (FGR) in patients with chronic hypertension is to perform serial ultrasound examinations to monitor fetal growth every three to four weeks. We initiate sonographic screening for FGR at 28 to 32 weeks but will perform an earlier examination if there is a clinical suspicion of FGR (eg, size << dates).

Despite the consistent association between chronic hypertension and SGA in meta-analyses, the optimal timing and frequency of screening for FGR have not been determined. Furthermore, while it is generally accepted that detection of FGR and intervention (close monitoring, early delivery) will improve perinatal outcomes, several observational studies have failed to show a reduction in perinatal mortality [68-70] and others report that 75 to 80 percent of SGA newborns may not be detected antenatally [71]. (See "Fetal growth restriction: Screening and diagnosis" and "Fetal growth restriction: Evaluation".)

Tests to monitor fetal well-being — We take the following approach to fetal surveillance in pregnancies complicated by chronic hypertension, while acknowledging the high degree of uncertainty regarding preferred strategies for optimizing perinatal outcomes:

●Kick counts – We suggest daily assessment of fetal kick counts starting at 28 weeks of gestation; <10 fetal movements in two hours should prompt further assessment of fetal well-being. Maternal assessment of fetal movement, or fetal kick counts, is an inexpensive and easily implemented method to assess fetal well-being and, when normal, generally reassuring to mothers; however, its value for reducing perinatal mortality is unproven. (See "Decreased fetal movement: Diagnosis, evaluation, and management".)

●NST, BPP – As chronic hypertension has been consistently demonstrated to confer an increased risk for stillbirth (see 'Fetal/neonatal risks' above) and most studies have not distinguished between severe or mild hypertensive disease, we perform routine fetal surveillance on all pregnancies complicated by chronic hypertension. We initiate twice weekly fetal surveillance at 32 weeks of gestation because routine surveillance implemented earlier in gestation is unlikely to improve perinatal outcomes [72]. Twice weekly rather than weekly fetal testing is performed routinely based on limited evidence suggesting a reduction in fetal deaths with frequent testing [73]. Testing may be started earlier and performed more frequently in patients thought to be at high risk of early stillbirth. ACOG recommends antenatal fetal surveillance for pregnant individuals with chronic hypertension who need medication or who have fetal growth restriction, superimposed preeclampsia, or underlying medical conditions that may affect fetal outcome, as these pregnancies are at increased risk for fetal demise [74,75]. For patients with hypertension that is well-controlled with medication, they suggest weekly testing beginning at 32 weeks; initiation and frequency of testing are individualized for patients with poorly controlled hypertension.

Comparison of serial nonstress tests (NSTs), biophysical profiles (BPPs), or modified BPPs reveals no significant difference in perinatal mortality rates associated with any specific modality of fetal surveillance [76]. The choice among these tests should be based on provider preference and other local factors.

●Umbilical artery Doppler – In pregnancies with FGR, management based on umbilical artery Doppler ultrasound findings is recommended as it has been demonstrated to reduce perinatal mortality [77-79]. (See "Fetal growth restriction: Evaluation" and "Fetal growth restriction: Evaluation", section on 'Umbilical artery Doppler'.)

Delivery

Timing

●We suggest delivery at 39+0 to 39+6 weeks of gestation for patients with well-controlled chronic hypertension alone and no indications for earlier delivery (eg, uncontrolled hypertension, superimposed preeclampsia, previous stillbirth, abruption in the current or past pregnancy, FGR).

An analysis of perinatal outcome data from over 170,000 patients with chronic hypertension (both with and without superimposed preeclampsia) concluded that delivery at 38+0 to 39+6 weeks appeared to provide the optimal trade-off between the risk of adverse fetal and adverse neonatal outcomes [80]. We prefer to wait until 39 weeks because of the clearly demonstrated risks associated with iatrogenic delivery before 39+0 weeks [81,82] and the increased likelihood of more favorable perinatal outcomes in patients with chronic hypertension alone.

ACOG suggested the following approach for delivery of patients with chronic hypertension [2]:

•≥38+0 to 39+6 weeks of gestation for patients not requiring medication

•≥37+0 to 39+0 weeks for patients with hypertension controlled with medication

•34+0 to 36+6 weeks for patients with severe hypertension that is difficult to control

The ranges allow for clinician judgment on a case-by-case basis, with consideration of factors such as steady-state levels of and trends in blood pressure, fetal growth and amniotic fluid volume, and cervical status. The Society of Obstetricians and Gynaecologists of Canada also states that patients with uncomplicated preexisting hypertension who are otherwise well should be considered for delivery at 38+0 to 39+6 weeks of gestation [83].

For patients with superimposed preeclampsia or other pregnancy complications, the timing of delivery should be decided on a case-by-case basis based on the type and severity of these complications. (See 'Patients with superimposed preeclampsia' below and "Acute placental abruption: Management and long-term prognosis" and "Stillbirth: Incidence, risk factors, etiology, and prevention" and "Fetal growth restriction: Pregnancy management and outcome", section on 'Delivery'.)

Intrapartum care

●General principles – Intrapartum management of patients with chronic hypertension should be driven by the same principles guiding intrapartum management in the general obstetric population. Cesarean birth should be reserved for standard obstetric indications. (See "Labor and delivery: Management of the normal first stage".)

●Treatment of hypertension – The goal of intrapartum blood pressure management is to prevent maternal cerebrovascular or coronary events while minimizing rapid fluctuations in blood pressure that could influence uterine perfusion [61]. Antihypertensive medication regimens started prior to labor should be continued intrapartum. Rapid-acting medications should be used for confirmed blood pressures ≥160 mmHg systolic or ≥110 mmHg diastolic; intravenous labetalol is our preferred first-line agent (table 6) [3]. ACOG endorses use of immediate-release oral nifedipine as a first-line option for emergency treatment of acute, severe hypertension in pregnancy, particularly when intravenous access is not in place.

●Fluids – Volume status (fluid intake and output) should be recorded, with the goal of maintaining euvolemia. Maintenance of euvolemia during labor is particularly important in patients with a long-standing history of hypertension and left ventricular hypertrophy and/or diastolic dysfunction, as they are predisposed to pulmonary edema with volume overload, whereas volume depletion can lead to tachycardia and reduced filling times, exacerbating any preexisting diastolic dysfunction.

●Magnesium sulfate – Intrapartum magnesium sulfate therapy for seizure prophylaxis is not indicated in the absence of superimposed preeclampsia as the risk of having a seizure is less than 0.1 percent [84].

In patients with hypertension related to chronic kidney disease who are preterm and receiving magnesium sulfate for neonatal neuroprotection, close maternal monitoring is essential for prevention and early recognition of magnesium toxicity. (See 'Management' below and "Preeclampsia: Intrapartum and postpartum management and long-term prognosis", section on 'Signs of magnesium toxicity'.)

Patients with superimposed preeclampsia

Definition/diagnostic criteria — Preeclampsia is considered superimposed when it occurs in a patient with previously diagnosed chronic hypertension. However, distinguishing superimposed preeclampsia from third-trimester physiologic increases in blood pressure and proteinuria can be challenging.

Superimposed preeclampsia is likely when any of the following are present:

●A sudden increase in blood pressure that was previously well-controlled or a need for a rapid escalation of antihypertensive medications to control blood pressure.

●The new onset of proteinuria or a sudden increase in proteinuria in a patient with known prepregnancy or early pregnancy proteinuria. A sudden increase in proteinuria is not precisely defined by various societies or in the existing literature. Based on limited evidence, we typically diagnose superimposed preeclampsia when the level of proteinuria increases 100 percent from baseline in patients with preexisting kidney disease or proteinuria [85].

The presence of any of the following severe features of preeclampsia supports the diagnosis of superimposed preeclampsia with severe features:

●Severely elevated blood pressure despite increasing antihypertensive therapy.

●Thrombocytopenia (platelet count <100,000/microliter).

●Elevated transaminases (two times the upper limit of the normal concentration for a particular laboratory) or severe persistent right upper quadrant or epigastric pain unresponsive to medication and not accounted for by alternative diagnoses, or both.

●New-onset or worsening renal insufficiency.

●Pulmonary edema.

●Persistent cerebral or visual disturbances.

In the absence of severe features, there may be ambiguity in the diagnosis of superimposed preeclampsia. Given the risk of disease progression and adverse outcomes, increased vigilance is recommended whenever the diagnosis is suspected.

Incidence and risk factors — Superimposed preeclampsia develops in 13 to 40 percent of pregnant patients with chronic hypertension. The risk for developing superimposed preeclampsia is higher in patients with long-standing, severe, or secondary hypertension; obesity; Black race; history of preeclampsia; and smoking [24].

Clinical presentation and evaluation — The clinical presentation of superimposed preeclampsia is similar to that in patients without chronic hypertension, and their evaluation should be the same. (See "Preeclampsia: Clinical features and diagnosis", section on 'Clinical presentation' and "Preeclampsia: Clinical features and diagnosis", section on 'Patient evaluation'.)

Results of laboratory testing should be compared with baseline information obtained early in pregnancy. As discussed above, new-onset proteinuria or a sudden large increase in protein excretion along with one or more features of severe disease strongly supports the diagnosis. However, in patients with long-standing kidney disease or kidney disease of unknown duration, changes in creatinine level and proteinuria should be cautiously interpreted before making a definitive diagnosis of superimposed preeclampsia. (See "Hypertensive disorders in pregnancy: Approach to differential diagnosis".)

Management — Upon diagnosis of superimposed preeclampsia, management of patients with chronic hypertension is generally similar to that of other patients with preeclampsia. (See "Preeclampsia: Antepartum management and timing of delivery".)

Some considerations for patients with superimposed preeclampsia include:

●Patients with superimposed preeclampsia should initially be monitored in the inpatient setting. If there are no severe features, outpatient monitoring may be considered if the patient remains stable, has no severe features of preeclampsia, and is able to comply with self-monitoring and frequent visits. While outpatient care after a period of inpatient monitoring may be a reasonable option for patients with superimposed preeclampsia without severe features, those with severe features should be in the hospital until delivery.

●As in patients with preeclampsia, administration of a course of antenatal corticosteroids to preterm gestations and antihypertensive therapy to patients with severe hypertension are important considerations. (See "Preeclampsia: Antepartum management and timing of delivery", section on 'Components of expectant management'.)

●Timing and indications for delivery with superimposed preeclampsia are based on gestational age, disease severity, progression of disease, and results of ongoing assessment of maternal and fetal well-being. With any attempts to prolong pregnancy, the potential neonatal benefits must be weighed against the risk of maternal harm. (See "Preeclampsia: Antepartum management and timing of delivery".)

Data from small retrospective studies of patients with preterm superimposed preeclampsia with severe features suggest that outcomes with expectant management are similar to those in patients with preterm preeclampsia with severe features alone [86,87]. Although these studies are small and limited by their study design, it appears that a similar approach to management is reasonable. (See "Preeclampsia with severe features: Delaying delivery in pregnancies remote from term".)

●The frequency of eclampsia in patients with superimposed preeclampsia is not well-defined but was up to 2.4 percent in observational and retrospective studies [24,86]. We administer magnesium sulfate peripartum for seizure prophylaxis to patients who have superimposed preeclampsia with severe features. In patients with chronic kidney disease on magnesium sulfate for prevention of seizures or fetal/neonatal neuroprotection, close maternal monitoring is essential for prevention and early recognition of magnesium toxicity. (See "Preeclampsia: Intrapartum and postpartum management and long-term prognosis", section on 'Seizure prophylaxis' and "Preeclampsia: Intrapartum and postpartum management and long-term prognosis", section on 'Signs of magnesium toxicity'.)

●Intrapartum and postpartum, volume status and fluid management are of particular importance as increased third-spacing from preeclampsia may predispose to pulmonary edema. (See "Preeclampsia: Intrapartum and postpartum management and long-term prognosis", section on 'Fluids'.)

Recurrence risk — Reports regarding the recurrence risk of superimposed preeclampsia are variable. In one study that was based on a secondary analysis of a larger antioxidant trial, patients with chronic hypertension and prior preeclampsia/HELLP/eclampsia had a 1.95-fold increase in risk of superimposed preeclampsia in a subsequent pregnancy compared with patients without prior preeclampsia/HELLP/eclampsia [24]. In contrast, a secondary analysis of a United States-based antioxidant trial found that the risk of superimposed preeclampsia was similar (28 percent, adjusted RR 1.28, 95% CI 0.78-2.11) in patients with chronic hypertension and prior preeclampsia versus those with no prior preeclampsia [88]. The risks for placental abruption, perinatal death, and SGA newborn were also similar for the two groups, but patients with prior preeclampsia had a higher rate of preterm birth <37 weeks (36.9 versus 27.1 percent) and at 34 to 36 weeks (30.9 versus 18.3 percent). Counseling regarding future pregnancy risk can be based on these data and those available for chronic hypertension in pregnancy overall.

POSTPARTUM CARE

Analgesia — The decision to use nonsteroidal anti-inflammatory drugs (NSAIDs) for analgesia should be individualized as these drugs are known to cause elevations in blood pressure in some nonpregnant individuals with hypertension. (See "NSAIDs and acetaminophen: Effects on blood pressure and hypertension".)

Overall, the body of data supports the safe use of NSAIDs in postpartum patients with blood pressure issues [89] and their use in patients with hypertension is supported by the American College of Obstetricians and Gynecologists [90]. If blood pressure is elevated in the postpartum period, we use acetaminophen as our first-line medication for pain management. NSAIDs should be used preferentially over opioid analgesics, when possible. However, we avoid post-delivery NSAID use in patients with preexisting kidney disease and/or elevated serum creatinine levels. (See "Treatment of hypertension in pregnant and postpartum patients", section on 'Management'.)

Blood pressure management — Blood pressure control is an ongoing issue during the postpartum period, even in patients with chronic hypertension who did not require antihypertensive therapy during pregnancy. Blood pressure often declines immediately after giving birth and continues to decline for a few days before increasing three to five days postpartum when the patient may already be at home [91]. The immediate decline is generally attributed to blood loss and the effects of analgesia, while the subsequent increase is likely due to mobilization of extravascular fluid with a rise in intravascular volume, as well as factors such as pain.

Early postpartum visits for a blood pressure check (within 3 to 10 days after giving birth [2]) or home blood pressure monitoring, particularly in the first two weeks postpartum, is recommended. Home blood pressure monitoring strategies are likely to be helpful given the often suboptimal compliance with postpartum visits [92]. The risk for developing severe hypertension postpartum was illustrated in a retrospective cohort study of 235 patients with chronic hypertension in which 13 percent developed severe hypertension postpartum [93]. At discharge, these patients had mean systolic and diastolic blood pressures of 141 and 78 mmHg, respectively, and 87 percent were discharged on antihypertensive medications.

Choice of medications for blood pressure control is the same as during pregnancy, or the patient's prepregnancy antihypertensive regimen can be resumed after delivery, with consideration of safety in breastfeeding when relevant. Dose adjustments of antepartum regimens may be needed to reflect the decrease in volume of distribution and glomerular filtration rate that occurs after giving birth [94]. If volume overload is suspected or diagnosed, then diuresis should be considered, such as with a brief course of furosemide. (See "Treatment of hypertension in pregnant and postpartum patients", section on 'Approach to patients with severe versus nonsevere hypertension'.)

Extended postpartum follow-up is important. A population-based retrospective cohort study found that postpartum hospitalization for cardiovascular disease (CVD) within one year after delivery was higher among patients with chronic hypertension than for normotensive patients (645 versus 136 per 100,000 delivery hospitalizations; adjusted hazard ratio 4.11, 95% CI 3.64-4.66) and the risk for readmission for CVD persisted for the entire year after giving birth [95]. (See 'Referral for primary care' below.)

Family planning — Contraception and appropriate timing of future pregnancies should be discussed. Estrogen-containing contraceptive agents are generally avoided in patients with stage 2 hypertension or higher (systolic blood pressure ≥140 mmHg or diastolic blood pressure ≥90 mmHg) even if well-controlled because the theoretic or proven risks generally exceed the benefits, and good alternatives are available. (See "Combined estrogen-progestin contraception: Side effects and health concerns", section on 'Eligibility criteria (WHO and CDC)'.)

Referral for primary care — Patients with known chronic hypertension should resume care with their primary care provider postpartum. Patients with chronic hypertension first diagnosed during pregnancy or in the postpartum period based on persistently elevated blood pressure 12 weeks after giving birth should be referred to a primary care provider for ongoing management of hypertension, which may persist or resolve. (See "Treatment of hypertension in pregnant and postpartum patients", section on 'Development of hypertension in nonpregnant patients after hypertension first presenting in pregnancy'.)

The pregnancy/postpartum time frame is an opportunity to educate patients regarding the long-term risks of hypertension and the importance of ongoing care, which may help to ensure follow-up with a primary care provider for long-term management of chronic hypertension and cardiovascular risks. Progression from mild to severe hypertension within seven years is common [96]. (See "Overview of hypertension in adults".)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Hypertensive disorders of pregnancy".)

SUMMARY AND RECOMMENDATIONS

●Diagnosis – Blood pressure criteria for hypertension in pregnancy are systolic blood pressure ≥140 mmHg, diastolic blood pressure ≥90 mmHg, or both. Severe hypertension is defined as systolic blood pressure ≥160 mmHg, diastolic blood pressure ≥110 mmHg, or both. Diagnostic definitions/criteria for the various hypertensive disorders related to pregnancy are described in the table (table 2). (See 'Definition/diagnostic criteria' above.)

The diagnosis of superimposed preeclampsia is challenging in the absence of severe features of preeclampsia. Given the risk of disease progression and adverse outcomes, increased vigilance is recommended whenever the diagnosis is suspected. Management is the same as that in other patients with preeclampsia. (See 'Patients with superimposed preeclampsia' above.)

●Overview of management

•Preconception – Ideally, patients with chronic hypertension are assessed prior to conception to address the issues described in the table (table 3), in addition to routine preconception assessments. Maternal-fetal medicine consultation should be considered for counseling and management both preconception and during pregnancy. (See 'Preconception care' above.)

•Early pregnancy evaluations – Baseline laboratory and cardiac evaluation is repeated at the first prenatal visit (table 3), if not recently performed. In addition, accurate gestational dating is important since these pregnancies are at increased risk for developing fetal growth restriction (FGR) and undergoing obstetrically indicated preterm birth. (See 'Baseline clinical evaluation, laboratory testing, and preeclampsia prophylaxis' above.)

•Low-dose aspirin prophylaxis – Low-dose aspirin is recommended after 12 weeks of gestation for prevention of preeclampsia as these patients are at high risk of developing the disease. (See "Preeclampsia: Prevention", section on 'Low-dose aspirin'.)

•Monitoring for FGR and evaluation of fetal wellbeing – We monitor for FGR beginning at 28 to 32 weeks and initiate twice weekly nonstress tests or biophysical profiles at 32 weeks.

•Timing of delivery – We suggest delivery at 39+0 to 39+6 weeks of gestation for patients with well-controlled chronic hypertension alone and no standard indications for earlier delivery. (See 'Timing' above.)

•Use of intrapartum magnesium sulfate – Intrapartum magnesium sulfate therapy for seizure prophylaxis is not indicated in the absence of superimposed preeclampsia. Antihypertensive medication regimens started prior to labor should be continued intrapartum, and severe hypertension should be treated promptly (table 6). (See 'Intrapartum care' above.)

•Postpartum monitoring – Postpartum visits for a blood pressure check within 3 to 10 days after giving birth or home blood pressure monitoring is recommended as severe hypertension can develop after hospital discharge. (See 'Blood pressure management' above.)

●Treatment of hypertension

•Severe hypertension – Severe maternal hypertension (systolic blood pressure ≥160 mmHg or diastolic blood pressure ≥110 mmHg) should be pharmacologically treated in a timely manner to reduce the risk for stroke. Options for drug therapy are shown in the table (table 6). (See 'Severe hypertension' above.)

•Nonsevere hypertension – Our approach to women with nonsevere chronic hypertension depends on whether there is end-organ involvement. Oral antihypertensive therapy dosing is shown in the table (table 7). (See 'Nonsevere hypertension' above.)

No end-organ involvement:

-For patients with nonsevere hypertension, not on antihypertensive therapy, and with no end-organ involvement, we utilize 140/90 mmHg as the threshold for initiation of medical therapy for chronic hypertension in pregnancy. We use the fewest medications at the lowest effective dose to achieve this goal.

-For patients with nonsevere hypertension, on antihypertensive therapy, and with no end-organ involvement, our decision making is individualized. For most patients with well-controlled blood pressures on an antihypertensive medication regimen with a good safety profile, it is reasonable to continue medications to decrease the occurrence of severe hypertension. A target blood pressure range of 120 to 139/80 to 89 mmHg is reasonable. However, it is also reasonable to discontinue medications during the first trimester to minimize fetal exposure and restart them if blood pressures meet the 140/90 mmHg threshold. With this approach, close blood pressure monitoring is imperative, and the blood pressure changes, such as the decline in the midtrimester and rise in the third trimester, must be considered.

End-organ involvement:

-For patients with nonsevere hypertension and end-organ involvement, our target blood pressure is 120 to 139/80 to 89 mmHg.

●Pregnancy outcome – Chronic hypertension is associated with substantial maternal and fetal/neonatal morbidity and mortality (table 1). Superimposed preeclampsia increases the risk of adverse outcomes. (See 'Risks of chronic hypertension in pregnancy' above.)