Treatment of hypertension in pregnant and postpartum patients

INTRODUCTION — Hypertension (defined in this topic as systolic blood pressure ≥140 mmHg or diastolic blood pressure ≥90 mmHg), is a common complication of pregnancy and the incidence is increasing [1,2]. When severe (defined as systolic blood pressure ≥160 mmHg or diastolic blood pressure ≥110 mmHg), it can lead to stroke and death, but prompt recognition and treatment can reduce the risk of these complications [3].

When hypertension is diagnosed in a pregnant patient, the major issues are:

●Establishing a diagnosis

●Determining the threshold for initiating treatment and the target blood pressure

●Avoiding drugs with potentially adverse fetal effects

●Determining the optimum time for delivery

This topic will discuss issues related to the choice, use, and safety of antihypertensive drugs in pregnancy, focusing on treatment of pregnancy-related hypertension. Other aspects of pregnancy complicated by hypertension are reviewed in separate topics, including, but not limited to:

●(See "Chronic hypertension in pregnancy: Prenatal and postpartum care".)

●(See "Preeclampsia: Clinical features and diagnosis".)

●(See "Preeclampsia: Antepartum management and timing of delivery".)

●(See "Preeclampsia: Prevention".)

●(See "Eclampsia".)

●(See "Gestational hypertension".)

CLASSIFICATION OF HYPERTENSIVE DISORDERS IN PREGNANCY — The major hypertensive disorders that occur in pregnant and postpartum patients are described in the table (table 1). The International Society for the Study of Hypertension in Pregnancy (ISSHP) system is slightly different and described separately. (See "Preeclampsia: Clinical features and diagnosis", section on 'Definitions/diagnostic criteria'.)

TECHNIQUE FOR ACCURATE MEASUREMENT OF BLOOD PRESSURE

●Inform patients to avoid caffeine and nicotine within 30 minutes of blood pressure measurement as either can increase readings.

●Use an appropriate, standardized technique for blood pressure measurement.

●Measure blood pressure after five minutes of rest, with the patient sitting or in a semireclining position with the back supported, feet on the ground and legs not crossed, and the arm supported at heart level.

Blood pressure measured on the left arm with the patient in left lateral recumbency does not differ substantially from blood pressure that is measured in the sitting position, thus it may be used if a seated blood pressure is not feasible, such as in hospitalized patients [4].

●Use an appropriately sized cuff – A large adult cuff for patients with an upper-arm circumference of 35 to 44 cm and a thigh cuff if the upper-arm circumference is 45 to 52 cm. When the cuff is appropriately sized, the width of the bladder is 40 percent of the circumference and covers 80 percent of the area from the elbow to the shoulder.

Obtaining an accurate blood pressure measurement is especially challenging in individuals with significant obesity, especially when the distance from the elbow to the shoulder is shorter than average. Although not widely available, the use of specially designed "conical"-shaped cuffs may help address this problem [5].

●Use a properly calibrated device

•The mercury sphygmomanometer has long been considered the gold standard for measuring blood pressure. If an auscultatory method is used, the first audible sound (Korotkoff I) is the systolic pressure, and the disappearance of sound (Korotkoff V) is the diastolic pressure [6,7]. However, if sounds are audible with the cuff deflated, which can happen in pregnant patients, then the abrupt muffling of sound (Korotkoff IV) should be used [4].

•Automated devices can also be used for measuring blood pressure [8].

The British Hypertension Society and the European Society of Hypertension recommended that blood pressure measuring devices used in pregnant patients should be validated in this population because pregnancy-related hemodynamic and vascular changes can affect measurement. However, a meta-analysis of validation studies of devices for blood pressure measurement in pregnancy highlighted the limitations of the available information on this issue [9]. Although most devices passed a validation protocol to demonstrate statistical equivalence between these devices and the gold standard mercury sphygmomanometer in pregnant patients, only one-third did so without any protocol violations (ie, the specific criteria required for proper performance and statistical reliability).

●Confirm high blood pressure by repeating measurements over several minutes, hours, or days, depending on the clinical scenario (eg, gestational duration, severity of hypertension, prior blood pressures).

Self-measured blood pressure is useful for diagnosing white coat hypertension, detecting masked hypertension, and detecting new or worsening hypertension that develops between office visits. (See "Out-of-office blood pressure measurement: Ambulatory and self-measured blood pressure monitoring".)

Blood pressure measurement is reviewed in more detail separately. (See "Blood pressure measurement in the diagnosis and management of hypertension in adults".)

PRECONCEPTION MANAGEMENT OF CHRONIC HYPERTENSION — Women with sustained hypertension should receive preconception antihypertensive treatment to achieve the optimum blood pressure targets recommended for nonpregnant women. Preliminary studies suggest that higher mean arterial pressures prior to conception, even within the normal range, are associated with worse pregnancy outcomes [10]. However, preconception optimization of blood pressure has not been proven to have a significant impact on pregnancy outcomes.

When pregnancy is being considered, or when women are actively trying to conceive, the obstetrician/maternal-fetal medicine specialist, primary care provider, and patient need to consider the risks and benefits of continuing a stable antihypertensive drug regimen versus replacement with one or more of the few drugs preferred for use in pregnant patients (labetalol, nifedipine, hydralazine, methyldopa). The following synopsis describes our approach:

●Consider labetalol, nifedipine, hydralazine, or methyldopa – We generally prefer to treat patients with drugs with an established fetal safety profile before they conceive, as this reduces concerns about theoretic or known teratogenic effects in early pregnancy. It also avoids the need to develop a new, effective antihypertensive regimen in the first trimester in addition to the multiple other issues that arise at that time (eg, pregnancy discomforts, routine and selective screening, patient education and counseling, etc).

We generally begin therapy with either extended-release nifedipine or labetalol; the choice is based on patient characteristics, such as frequent headaches, resting heart rate, and exercise regimen (nifedipine may cause headaches while labetalol may reduce headache frequency, nifedipine may cause tachycardia in patients with a fast baseline heart rate while labetalol may block the physiologic increase in heart rate during vigorous exercise). If two drugs are needed, we generally use extended-release nifedipine and labetalol, but may use nifedipine and a diuretic in patients with salt-sensitive hypertension.

However, continuing the drug regimen until the patient has a positive pregnancy test and switching drugs at that time may be preferable in some cases, such as a patient with infertility who may take a long time to conceive or may not conceive or a patient who is particularly bothered by the side effects of the drugs preferred in pregnancy.

●Avoid ACE inhibitors, ARBs, MRAs – We recommend avoiding angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs) in women of childbearing age who are planning pregnancy and for whom reasonable effective alternatives exist that are safer for the fetus. We also recommend avoiding these medications in those not planning pregnancy but may not correctly and consistently use effective contraception.

For patients on these medications, emphasizing very early detection of planned or unplanned pregnancy is important so that the drug can be promptly discontinued and thus minimize embryonic exposure (unless hypertension is refractory to other safer antihypertensive medications [11]). ACE inhibitors and ARBs should not be used in the second or third trimester because they interfere with fetal renal hemodynamics. (See "Adverse effects of angiotensin converting enzyme inhibitors and receptor blockers in pregnancy".)

We also recommend not using mineralocorticoid receptor antagonists (MRAs; eg, spironolactone, eplerenone) because of safety concerns and limited pregnancy information. (See 'Mineralocorticoid receptor antagonists' below.)

●Preferred calcium channel blockers – For patients on a commonly used calcium channel blocker such as amlodipine, we suggest switching to extended-release or intermediate-acting nifedipine before conception since more fetal safety data are available for nifedipine and a network meta-analysis suggested nifedipine was more likely to prevent severe hypertension in pregnancy compared with other commonly used medications in pregnancy [12]. A patient in whom hypertension is well controlled by amlodipine is likely to respond equally well to intermediate-acting or extended-release nifedipine, although side effect profiles are slightly different. (See 'Calcium channel blockers' below.)

●Preferred beta blockers – For patients on a commonly used beta blocker such as carvedilol, we suggest switching to labetalol before conception. Both beta blockers have alpha-blocking activity and are likely to be similarly effective, but much more and generally reassuring pregnancy data are available for labetalol.

We avoid atenolol (a beta-1 selective blocker) because of recurring, but not definitive, reports of an association with fetal growth restriction. Metoprolol is also a beta-1 selective blocker but has not been associated with growth restriction in the same way as atenolol and is used more widely in pregnancy than atenolol. While we prefer metoprolol to atenolol for this reason, labetalol remains the preferred beta blocker in pregnancy. (See 'Beta blockers' below and 'Selected beta blockers: Atenolol and propranolol' below.)

●Use of thiazides – For patients on a thiazide or thiazide-like diuretic, we discuss discontinuing the drug or reducing the dose before conception or in early pregnancy, although there is no evidence of teratogenic effects or other adverse effects on pregnancy.

•If the diuretic is discontinued and blood pressure increases to a level warranting treatment, we begin labetalol, nifedipine, or methyldopa.

•If the diuretic dose is reduced and the blood pressure subsequently increases, we either increase the dose back up again or add a second drug such as labetalol, nifedipine, or methyldopa.

When thiazide or thiazide-like diuretics are needed to control hypertension, such as in patients who require a two- or three-drug regimen and are salt-sensitive, we are comfortable continuing these drugs during pregnancy, albeit with close monitoring and prescribing the lowest dose needed to control hypertension. Although theoretic concerns have been raised about the impact of diuretics on the normal physiologic plasma volume expansion in pregnancy, most individuals on chronic diuretic therapy have reached a steady state with, in most cases, only very mild decreases in blood volume. Compensatory mechanisms such as increased dietary salt intake and stimulation of the renin angiotensin system often compensate for the mild volume depletion [13]. (See 'Thiazide diuretics' below.)

WHEN TO INITIATE ANTIHYPERTENSIVE THERAPY IN PREGNANCY — The decision to treat hypertension during pregnancy should consider the risks and benefits for both mother and fetus. The level of blood pressure and the immediate risks to maternal well-being are the most important initial considerations.

All patients with severe hypertension — There is consensus that pregnant/postpartum patients with severe hypertension (defined as systolic blood pressure ≥160 mmHg and/or diastolic blood pressure ≥110 mmHg) confirmed by a repeat measurement within 15 minutes should be treated promptly to reduce the risk of stroke, heart failure, and other serious maternal complications. Guidelines from the American College of Obstetricians and Gynecologists (ACOG) state that these patients should receive antihypertensive agents as soon as reasonably possible after the criteria for acute onset severe hypertension are met and within 30 to 60 minutes of diagnosis [14]. (See 'Acute therapy of severe hypertension' below.)

The following study highlights the need for prompt blood pressure control in pregnant and postpartum patients with severe hypertension and the impact of severe systolic hypertension, which appears to be more predictive of adverse cerebrovascular events than severe diastolic hypertension [15]. In this retrospective case series of 26 deaths due to stroke related to preeclampsia/eclampsia in which blood pressures before the event were available, systolic blood pressure was >160 mmHg in 96 percent of cases (25 out of 26) and diastolic blood pressure was ≥110 mmHg in 65 percent of cases (17 out of 26) and >105 mmHg in 73 percent of cases (19 out of 26) [15]. The authors identified a good-to-strong chance to alter outcome in two-thirds of cases, with delayed response to clinical warning signs (eg, headache) accounting for 91 percent of these cases. Less than one-half of the patients received any antihypertensive therapy before the stroke, and drug therapy was not optimal in most of these cases.

Patients with nonsevere hypertension (chronic or pregnancy-related)

Our approach — When deciding whether to treat mild hypertension (defined here as systolic blood pressure 140 to 149 mmHg and/or diastolic blood pressure 90 to 99 mmHg) or moderate hypertension (defined here as systolic blood pressure 150 to 159 mmHg and/or diastolic blood pressure 100 to 109 mmHg), our approach considers the potential risk for developing severe hypertension, the potential benefit of preventing severe hypertension, and the patient's comorbidities and symptoms (eg, headaches, visual disturbances).

●Pregnant patients with chronic nonsevere hypertension (based on medical history or systolic blood pressure of ≥140 mmHg or a diastolic blood pressure ≥90 mmHg or both on at least two occasions at least four hours apart before 20 weeks of gestation) – We recommend antihypertensive treatment for these patients, based on favorable findings from the CHAP trial discussed below [16], which was limited to patients with chronic hypertension. Drug choice, dosing, and target blood pressures are the same as those for maintenance therapy after acute treatment of severe hypertension, as discussed below. (See 'Oral maintenance therapy' below and 'Target blood pressure' below.)

●Patients with pregnancy-related nonsevere hypertension (gestational hypertension, preeclampsia)

•Systolic 150 to 159 mmHg and/or diastolic 100 to 109 mmHg – For antepartum patients with new-onset hypertension after 20 weeks of gestation (ie, gestational hypertension or preeclampsia) with blood pressures at this level that persist after multiple inpatient or outpatient blood pressure measurements over a short period of time, we initiate (or increase existing) antihypertensive therapy if delivery is likely to be delayed for more than 24 hours. Our decision to treat nonsevere hypertension is consistent with some guidelines [17] and data that a threshold of ≥155/105 mmHg was good to excellent at identifying patients at increased risk of adverse maternal central nervous system outcome, stillbirth, and perinatal death [18].

Drug choice, dosing, and target blood pressures are the same as those for maintenance therapy after acute treatment of severe hypertension, as discussed below. (See 'Oral maintenance therapy' below and 'Target blood pressure' below.)

•Systolic 140 to 149 and/or diastolic 90 to 99 mmHg – For antepartum patients with new-onset hypertension after 20 weeks of gestation (ie, gestational hypertension or preeclampsia) and persistent blood pressures at this level, we strongly consider initiating antihypertensive therapy if delivery is likely to be delayed for several days or weeks. If blood pressure increases over a short time, symptoms (particularly headache) may occur even in young patients with pressures <150/100 mmHg. The decision to begin treatment is based on individual patient factors and shared decision-making. Some guidelines consider the threshold for treatment of hypertension in pregnancy to be systolic pressure ≥140 mmHg and/or a diastolic pressure ≥90 mmHg, whether the hypertension is chronic, gestational, or due to preeclampsia [17], whereas some clinicians would not treat patients with nonsevere hypertension so as not to mask the onset of preeclampsia with severe features.

Drug choice, dosing, and target blood pressures are the same as that for maintenance therapy after acute treatment of severe hypertension, as discussed below. (See 'Oral maintenance therapy' below and 'Target blood pressure' below.)

•Systolic 130 to 139 mmHg and/or diastolic 80 to 89 mmHg – We consider initiation of treatment at this blood pressure level in two groups of patients: (1) antepartum adolescents and other patients whose baseline blood pressures were low (baseline less than 90/75 mmHg) and (2) patients with signs of heart failure (eg, chest discomfort, shortness of breath) or cerebrovascular symptoms (eg, headache, visual disturbances, confusion), but we acknowledge that this approach is not evidence based. Some clinicians would not treat these patients so as not to mask the onset of preeclampsia with severe features.

Although the traditional approach in the United States is to only begin antihypertensive treatment of gestational hypertension and preeclampsia when blood pressure is severely elevated (systolic ≥160 mmHg and/or diastolic ≥110 mmHg) [11], in an analysis of 24 patients with stroke related to preeclampsia, 4 percent had systolic blood pressures below severe levels (ie, >155 mmHg and <160 mmHg), which supports our lower threshold for initiating therapy [19]. Furthermore, evidence suggests that the pathophysiology of the neurologic manifestations of eclampsia is similar to that of the posterior reversible encephalopathy syndrome [20]. If this is the case, then patients with preeclampsia may be more susceptible to the neurologic features of severe disease at lower blood pressures (eg, systolic ≥150 rather than ≥160 mmHg ), and this would support beginning antihypertensive therapy at a lower threshold in these patients.

In 2022, a scientific statement from the American Heart Association, which included the author of this topic, concluded that consistent evidence that antihypertensive therapy for pregnancy hypertension of any type halves the incidence of severe hypertension and may be a sufficiently compelling reason for more aggressive treatment of nonsevere hypertension in pregnancy, particularly in under-resourced communities with less experience and low capacity to respond to hypertensive urgencies and emergencies that could result in serious hypertensive end-organ complications [21].

Review of evidence — Pharmacotherapy of nonsevere hypertension is more controversial than for severe hypertension [22] and the threshold for initiating antihypertensive treatment varies by specific diagnosis and by guideline. In 2022, the Chronic Hypertension and Pregnancy trial (CHAP, discussed below) reported improved pregnancy outcomes in participants treated at a threshold of 140/90 mmHg compared with those treated at a threshold of 160/105 mmHg [16]. This finding resulted in more widespread agreement regarding treatment of nonsevere chronic hypertension in pregnancy. However, treatment of nonsevere pregnancy-related hypertension remains controversial given uncertainty about the benefits of lowering blood pressure over the relatively short duration of pregnancy, potential fetal risks from drug-related reductions in uteroplacental blood flow, and potential teratogenic effects of antihypertensive drugs [21].

Benefits in patients with chronic hypertension — The Control of Mild Hypertension During Pregnancy Trial (CHAP) evaluated treatment of mild chronic hypertension during pregnancy, based on a systolic blood pressure of ≥140 mmHg or a diastolic blood pressure ≥90 mmHg or both on at least two occasions at least 4 hours apart before 20 weeks of gestation or based on medical history of chronic hypertension and past/present antihypertensive therapy [16]. For patients with a history of chronic hypertension but not receiving antihypertensive drug therapy within 24 hours before measurement, a systolic pressure of 140 to 159 mmHg or a diastolic pressure of 90 to 104 mmHg was required. For patients with a history of chronic hypertension and receiving antihypertensive therapy, a systolic pressure of <160 mmHg and a diastolic pressure of <105 mmHg were required.

The 2408 participants were randomly assigned to a blood pressure goal of <140/90 mmHg (active treatment group) or to usual care (control group) where antihypertensive therapy was withheld or stopped at randomization unless severe hypertension developed (systolic pressure ≥160 mmHg or diastolic pressure ≥105 mm Hg), in which case they were begun on antihypertensive therapy and the goal blood pressure was also <140/90 mmHg. Active treatment resulted in:

●Reduction of the composite outcome (preeclampsia with severe features, medically indicated preterm birth <35 weeks, abruption, or fetal or neonatal death: 30.2 versus 37.0 percent, risk ratio [RR] 0.82, 95% CI 0.73-0.92). Viewed individually, each of these outcomes was reduced, but only the reductions in preeclampsia with severe features (23.2 versus 29.1, RR 0.80, 95% CI 0.70-0.92) and medically indicated preterm birth <35 weeks (12.2 versus 16.7 percent, RR 0.73, 95% CI 0.60-0.89) were statistically significant.

●Reduction in any preeclampsia (24.4 versus 31.1 percent, RR 0.79, 95% CI 0.69-0.89)

●Reduction in preterm birth <37 weeks (27.5 versus 31.4 percent, RR 0.87, 95% CI 0.77-0.99)

●Reduction in severe hypertension (36.1 versus 44.3 percent, RR 0.82, 95% CI 0.74-0.90)

●No increase in risk for small-for-gestational-age (SGA) birth weight (<10^th percentile) (11.2 versus 10.4 percent, aRR 1.04, 95% CI 0.82-1.31).

Planned secondary analysis of these data evaluated the subgroup of women with mean clinic blood pressures <140/90 mmHg after randomization [23]. Those with mean clinic systolic and diastolic blood pressures <130/80 mmHg were compared with those with mean systolic and diastolic blood pressures of 130-139/80-89 mmHg. The primary outcome was the same composite measure used in the CHAP trial and was reduced by more than half in the group with mean systolic and diastolic blood pressures <130/80 mmHg (16 versus 36 percent; adjusted RR 0.45, 95% CI 0.38-0.54).

Benefits in mixed populations of patients with chronic or pregnancy-related hypertension — Several meta-analyses of randomized trials of treatment versus no treatment of pregnant patients with nonsevere hypertension published prior to the CHAP trial provided the following key findings. In contrast to CHAP, these trials included mixed populations of patients with chronic and pregnancy-related hypertension.

●Prevention of severe hypertension – In meta-analyses of randomized trials of antihypertensive therapy versus no therapy of nonsevere hypertension in pregnancy, treatment reduced the incidence of severe hypertension by 40 to 70 percent compared with placebo [24-26]. Severe hypertension is known to be associated with severe maternal morbidity and mortality, and prevention and treatment of severe hypertension is acknowledged by most professional societies to be important and beneficial [14,24,27]. Although the meta-analyses did not find a significant reduction in stroke, this is most likely explained by the extremely low frequency of stroke in the study populations, treatment of severe hypertension when diagnosed, and lack of power to detect a difference in this outcome. Individual trials in pregnant patients with gestational or chronic hypertension have suggested a benefit. In the Control of Hypertension in Pregnancy trial (CHIPS), less tight diastolic blood pressure control (100 mmHg) resulted in a higher rate of severe hypertension than tight control (85 mmHg) [28] and, in post hoc analysis, severe hypertension was associated with a greater risk of subsequent adverse maternal outcome, after adjustment for allocated group, prognostic factors, and preeclampsia [29].

●Other outcomes – Severe maternal hypertension has been associated with higher rates of preterm birth, preeclampsia, features of HELLP syndrome, and low birth weight [27]. However, in meta-analyses of randomized trials of antihypertensive therapy versus no therapy of nonsevere hypertension in pregnancy, treatment generally did not reduce the occurrence of preeclampsia, perinatal death, preterm birth, or placental abruption, although heterogeneity in study designs limit interpretation of these findings [24-26]. In CHIPS, less tight diastolic blood pressure control (100 mmHg) resulted in more patients with thrombocytopenia or symptomatic elevated liver enzymes, but no difference in serious maternal complications [29]. Tight blood pressure control did not increase the frequency of small for gestational age newborns compared with less tight control, which is reassuring since optimal fetal growth depends, in part, on placental perfusion.

ACUTE THERAPY OF SEVERE HYPERTENSION

Choice of therapy — We suggest labetalol or hydralazine administered intravenously as a first-line agent for acute therapy of severe hypertension. The author prefers to limit use of oral immediate-release rapid-acting nifedipine as a first-line option to patients in whom intravenous access is not readily available (algorithm 1) because a rapid large reduction in blood pressure may occur (see 'Nifedipine' below), whereas the American College of Obstetricians and Gynecologists (ACOG) considers labetalol, hydralazine, or immediate-release rapid-acting nifedipine similarly safe and effective as first-line options for urgent treatment of acute, severe hypertension [14], supported by several meta-analyses [30-34]. A systematic review of drugs for treatment of very high blood pressure in pregnancy concluded that the choice of antihypertensive should depend on the clinician's experience and familiarity with a particular drug, with consideration of its adverse effects and patient preferences; however, it is probably best to avoid use of nimodipine, diazoxide, and ketanserin (no longer actively marketed worldwide) [30].

We do not consider race a factor in drug choice. Although some experts choose different drug classes for monotherapy in Black patients as compared with other patients, the evidence supporting that approach is based on trials in nonpregnant adults and may not apply to pregnant patients. (See "Choice of drug therapy in primary (essential) hypertension", section on 'Role of patient race in selection of initial monotherapy'.)

Dosing — Drug dosing is described below and summarized in the table (table 2). During acute therapy, the fetal heart rate is monitored continuously if the fetus is viable.

Labetalol — We suggest intravenous labetalol for first-line therapy because it is effective, has a rapid onset of action (five minutes or less), and has a good safety profile [35-37]. Asthma requiring medication or maternal heart rate <60 beats/minute is a contraindication to use, whereas labetalol is preferred to other classes of antihypertensive drugs if the maternal heart rate >110 beats/minute.

●Begin with 20 mg intravenously over 2 minutes followed at 10-minute intervals by doses of 20 to 80 mg up to a maximum total cumulative dose of 300 mg if blood pressure remains above target level. As an example, give 20 mg, then 40 mg, then 80 mg, then 80 mg, then 80 mg. A constant infusion of 1 to 2 mg/minute can be used instead of intermittent therapy. Continuous cardiac monitoring is not necessary routinely but should be used in patients with relevant comorbidities (eg, coronary artery disease).

●The fall in blood pressure begins within 5 to 10 minutes and lasts from three to six hours.

●Although manufacturer's labeling recommends against exceeding a 300 mg cumulative dose (intermittent intravenous and continuous infusion), it may be reasonable to exceed this threshold in closely monitored patients who are responding and have a heart rate ≥60 beats/minute [38].

●If labetalol alone is ineffective, we suggest switching to hydralazine. Alternatively, intravenous nicardipine or oral nifedipine can be used.

Additional information on beta blockers is provided below. (See 'Beta blockers' below.)

Hydralazine

●Begin with 5 mg intravenously over 1 to 2 minutes; if the blood pressure goal is not achieved within 20 minutes, give a 5 to 10 mg bolus depending on the initial response.

●The fall in blood pressure begins within 10 to 30 minutes and lasts from two to four hours.

●If a total cumulative dose of 20 to 30 mg per treatment event does not achieve optimal blood pressure control or heart rate exceeds 100 beats/minute, another agent should be used.

●If hydralazine is ineffective, we suggest switching to labetalol.

Additional information on hydralazine is provided below. (See 'Hydralazine' below.)

Nifedipine

Choosing between immediate- and intermediate-/extended-release formulations — The author limits use of immediate-release rapid-acting nifedipine to patients with severe (≥160/110 mmHg) and symptomatic hypertension who require an immediate (in less than 30 minutes) decrease in blood pressure and in whom intravenous access is not readily available.

In less acute settings, the author's preference is to select one of the intermediate-acting or extended-release formulations when using a calcium channel blocker [39-41]. The extended-release preparations lower blood pressure more slowly (within 60 minutes rather than within 5 or 10 minutes), and in many cases, this time frame is sufficient. She prefers these formulations because of concern about the effects of rapid and severe blood pressure reduction that can occur with immediate-release rapid-acting nifedipine. These effects include reduction in uteroplacental perfusion and reflex activation of the maternal sympathetic nervous system causing increases in heart rate and headaches; more serious adverse cardiovascular events (stroke, myocardial infarction, arrhythmias) have been reported in older adults.

There is limited information comparing the different formulations in pregnancy.

●In a trial from Australia comparing 10 mg nifedipine tablets (slow release intermediate acting) with 10 mg capsules (immediate release) for acute treatment of severe hypertension in pregnancy at 45 and 90 minutes, patients who received the immediate-release capsules had a significantly greater fall in blood pressure and a rise in heart rate compared with those who received slow-release intermediate-acting tablets [42]. More patients who received tablets required a second dose because of persistent hypertension after 45 minutes, but most patients in both groups achieved target blood pressures by 90 minutes.

●A meta-analysis compared randomized trials of oral nifedipine versus intravenous labetalol [40]. Seven trials (four from resource-limited countries) with a total of 363 mother-infant pairs were included; four of the nifedipine trials used the slow-release intermediate-acting tablets and one used immediate-release nifedipine capsules. The pooled analysis found that, compared with intravenous labetalol, oral nifedipine had less risk of persistent hypertension (relative risk [RR] 0.42, 95% CI 0.18–0.96) and fewer maternal side effects (RR 0.57, 95% CI 0.35–0.94); however, on sensitivity analysis the outcome persistent hypertension was no longer significant. Although other outcomes did not reach statistical significance, one of 176 patients in the nifedipine group developed hypotension (systolic blood pressure <90 mmHg and/or diastolic blood pressure <60 mmHg) versus zero of 167 patients in the labetalol group and this patient was one of the 25 patients who received immediate-release nifedipine [43].

●In a meta-analysis comparing oral nifedipine to other antihypertensive medications for management of hypertensive disorders of pregnancy, use of oral nifedipine resulted in reduction in time required to achieve target blood pressure (standardized mean difference [SMD] -0.61, 95% CI -1.02 to -0.19; 14 trials, 1212 participants) and fewer doses were required (SMD 0.58, 95% CI -0.89 to -0.26; 12 trials, 1002 participants) [44]. Headache was more common in the nifedipine group (RR 1.75, 95% CI 1.29-2.37; 15 trials, 1218 participants). The risk of hypotension was not significantly increased (RR 1.29, 95% CI 0.48-3.41; 9 trials, 803 participants). Immediate release nifedipine was used in all but one trial (this trial used slow release) and labetalol was the comparator in most trials (other comparators were hydralazine, nitroglycerin, and prazosin).

Dosing

●Immediate-release rapid-acting capsule (10 mg) lowers blood pressure within 20 minutes. In the United States, the US Food and Drug Administration (FDA) package insert notes that, "Nifedipine capsules should not be used for the acute reduction of blood pressure" [45]. As discussed above, the author cautions against its routine use, whereas ACOG considers labetalol, hydralazine, or immediate-release rapid-acting nifedipine similarly safe and effective as first-line options for urgent treatment of acute, severe hypertension [14].

•A common dose is 10 mg orally initially

•If target blood pressure is not achieved in 20 minutes, administer 10 to 20 mg depending on initial response and repeat blood pressure 20 minutes later.

•If target blood pressure is still not achieved, administer another 10 to 20 mg depending on previous responses.

•If target blood pressure is still not achieved in 20 minutes, then switch to another agent (eg, intravenous labetalol).

In one trial that included 30 pregnant patients with sustained severe hypertension (mean 165/108 mmHg), a median of two doses was required for control of blood pressure [46].

●Extended-release tablet (30 mg) lowers blood pressure within one to two hours, lasts 24 hours, and is known as nifedipine XL or CR or ER. This formulation is less likely to result in a rapid and severe fall in blood pressure than the short-acting capsule.

If the target blood pressure is not achieved in one to two hours, a second dose can be administered.

●Intermediate-acting tablet (10 or 20 mg; in some countries, this is known as nifedipine retard) has a more delayed onset than the immediate-release rapid-acting capsule.

Additional information on nifedipine is available below. (See 'Calcium channel blockers' below.)

Target blood pressure — Once treatment is initiated, we attempt to reduce mean arterial pressure by no more than 25 percent over two hours to achieve target blood pressures of 130 to 150 mmHg systolic and 80 to 100 mmHg diastolic. We caution against aggressively lowering blood pressure (eg, <120/80) in such cases as this may reduce uteroplacental perfusion.

We believe our approach is prudent, and acknowledge a lack of clinical trial data to support these recommendations and the need to individualize therapy based on maternal and fetal factors. The rapidity with which blood pressure should be brought to safe levels is controversial [47]. Cerebral or myocardial ischemia or infarction can be induced by aggressive antihypertensive therapy if the blood pressure falls below the range at which tissue perfusion can be maintained by autoregulation. (See "Management of severe asymptomatic hypertension (hypertensive urgencies) in adults".)

After achieving the target blood pressure, blood pressure should continue to be closely monitored (eg, for patients not in labor: every 10 minutes for the first hour, every 15 minutes for second hour, every 30 minutes for the third hour, and then every hour for four hours; intrapartum patients are monitored more frequently).

Treatment of hypertension refractory to first-line acute therapy — Rarely, blood pressure is not controlled with one or a combination of the drugs described above (labetalol, hydralazine, nifedipine). We suggest nicardipine or esmolol by infusion pump in these cases.

●Nicardipine – Nicardipine is a dihydropyridine calcium channel blocker, similar to nifedipine, and can be given intravenously. The initial dose of nicardipine is 5 mg/hour intravenously by infusion pump and can be increased to a maximum of 15 mg/hour.

A review of studies of intravenous nicardipine for treatment of severe hypertension in pregnancy found that target blood pressure was reached within 23 minutes in 70 percent of pregnant patients with severe hypertension and 91 percent reached target blood pressure within 130 minutes with no severe maternal or fetal side effects [48].

Another study that examined the uteroplacental and fetal circulations with Doppler in 10 severely hypertensive preeclamptic patients receiving intravenous nicardipine found that afterload reduction triggered an increase in cardiac output without reducing uteroplacental or fetal perfusion [49].

●Esmolol – Esmolol is a relatively cardioselective beta blocker with a short half-life and duration of action. No studies have described use of esmolol for treatment of preeclampsia, but it has been used in pregnant patients to control sympathetic hyperactivity from thyroid storm [50,51].

A reasonable dose is 250 to 500 mcg/kg over one minute, then initiate intravenous infusion at 25 to 50 mcg/kg per minute; titrate incrementally up to a maximum of 300 mcg/kg per minute.

Other options for selected cases:

●Nitroglycerin is an option for treatment of hypertension associated with pulmonary edema in the rare occasion when intravenous diuretics are not effective. It acts by providing nitric oxide, which then causes vasodilation of both arterioles and veins.

It may be given as an intravenous infusion of 5 mcg/minute and gradually increased every three to five minutes to a maximum dose of 100 mcg/minute [52].

●Nitroprusside is administered as a last resort. A reasonable dose is 0.25 to 10 mcg/kg per minute as an intravenous infusion for as short a time as possible and not to exceed 2 mcg/kg per minute. (See 'Nitroprusside' below.)

A more complete review of these drugs and potential side effects is available separately. (See "Drugs used for the treatment of hypertensive emergencies".)

Of note, magnesium sulfate, which is usually administered to patients with preeclampsia, eclampsia, or gestational hypertension with severe features, is never a substitute for prompt initiation of antihypertensive treatment of severe hypertension as it has minimal effects on blood pressure.

ORAL MAINTENANCE THERAPY — Oral antihypertensive therapy may be needed to maintain blood pressure in the target range in patients in whom antihypertensive therapy was initiated and delivery is not imminent. There is no consensus on the optimum target blood pressure range for these patients. Targets of 110 to 140/85, ≤135/85, <140/90, and 130 to 140/80 to 90 mmHg have been suggested and are reasonable [53-55].

Drug dosing is shown in the table (table 3). We prefer labetalol or intermediate-acting or extended-release nifedipine. Oral hydralazine may be added if needed to achieve and maintain target blood pressure (see 'Beta blockers' below and 'Calcium channel blockers' below and 'Hydralazine' below). Methyldopa is also acceptable, but many patients will not achieve blood pressure goals or are bothered by its sedative effect at high doses. (See 'Methyldopa' below.)

In a network meta-analysis of randomized trials comparing antihypertensives for nonsevere pregnancy hypertension, regardless of pregnancy hypertension type, labetalol appeared to reduce 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), although the absolute magnitude of the effect may not be clinically important [56].

POSTPARTUM PATIENTS

Normal postpartum blood pressure changes — Blood pressure may be lower or even normal immediately after birth. However, blood pressure then increases, peaks three to six days postpartum, and may be significantly higher in the postpartum period than antepartum or intrapartum.

Breastfeeding does not increase blood pressure in nursing mothers.

Postpartum hypertension — Postpartum hypertension has been observed in as many as 20 percent of patients within six weeks of giving birth [57]. Risk factors include a high body mass index and diabetes mellitus [57-59].

Etiology — Postpartum hypertension may be due to persistence of antepartum or intrapartum hypertension or may be of new onset. The possibility of postpartum preeclampsia should be considered; the signs and symptoms of preeclampsia are first recognized postpartum (ie, postpartum preeclampsia) in approximately 5 percent of preeclampsia cases, usually within 48 hours of delivery. (See "Preeclampsia: Clinical features and diagnosis", section on 'Typical presentation' and "Preeclampsia: Clinical features and diagnosis", section on 'Onset or exacerbation of symptoms >2 days postpartum'.)

Transient new-onset postpartum hypertension can be related to a combination of factors, including administration of a large volume of intravenous fluids to patients who have had a cesarean birth or neuraxial anesthesia for labor, loss of pregnancy-associated vasodilation after delivery, mobilization of extravascular fluid after delivery, administration of ergot derivatives for prevention or treatment of postpartum hemorrhage, and/or prolonged administration of high doses of nonsteroidal anti-inflammatory drugs (NSAIDs) for postdelivery analgesia [57,60].

Primary aldosteronism is a rare cause of postpartum hypertension. Individuals with this disorder may not have hypertension during pregnancy due to the natriuretic effects of progesterone, and then present with hypertension with or without hypokalemia after delivery [61]. (See "Pathophysiology and clinical features of primary aldosteronism" and "Diagnosis of primary aldosteronism".)

Evaluation — Patients with new-onset postpartum hypertension should be evaluated by history (including review of postpartum medications and fluid balance), physical examination, and laboratory studies (serum electrolytes, liver chemistries, platelet count, creatinine, urine protein) for preeclampsia and primary (and secondary) hypertension. The presence of neurologic, cardiac, or gastrointestinal symptoms or laboratory abnormalities suggests a disorder other than transient hypertension related to fluids and/or medications [62]. Postpartum preeclampsia is often associated with persistent headaches and/or visual changes. (See "Preeclampsia: Clinical features and diagnosis", section on 'Patient evaluation' and "Overview of hypertension in adults", section on 'Evaluation'.)

Management — New-onset postpartum hypertension with laboratory abnormalities consistent with preeclampsia should be managed as such, with treatment of maternal hypertension, close monitoring, and possibly magnesium sulfate to prevent convulsions. (See "Preeclampsia: Intrapartum and postpartum management and long-term prognosis", section on 'Patients with postpartum onset of preeclampsia'.)

Approach to patients with severe versus nonsevere hypertension

●Severe hypertension – Severe hypertension, especially when acute and associated with symptoms (headache, chest pain, or shortness of breath), requires treatment within a short period of time (eg, 30 to 60 minutes). Given the vulnerability of patients to peripartum stroke, we recommend lowering blood pressure with parenteral agents (labetalol, hydralazine, or nicardipine) or an oral calcium channel blocker (table 2). (See 'Acute therapy of severe hypertension' above.)

●Nonsevere hypertension – We also suggest antihypertensive therapy for patients with systolic blood pressure ≥140 mmHg and/or diastolic blood pressure ≥90 mmHg that persist after multiple blood pressure measurements, especially when the patient is ready to be discharged. Some guidelines use a higher threshold (eg, 150/100 mmHg [55]).

Although rare, strokes (both hemorrhagic and thrombotic) associated with pregnancy are more likely to occur in the postpartum period [63]. The majority of pregnancy-related strokes occur in the first 10 days after delivery [64] and typically within 48 hours postpartum, with hypertension the strongest risk factor [63]. Furthermore, there is little reason to withhold antihypertensive medication once patients are postpartum, and adverse fetal effects of antihypertensive therapy are not a concern unless they are incompatible with breastfeeding.

•Choice of antihypertensive drug – We use antihypertensive medications similar to those used for maintenance therapy in pregnancy since most obstetric providers are familiar with these medications and they are compatible with breastfeeding (table 3). One guideline suggests avoiding methyldopa postpartum because of the risk of postnatal depression [52]. High-quality evidence to guide optimum management of postpartum nonsevere hypertension is limited [65].

•Role of furosemide – Brief furosemide therapy (20 mg orally once or twice per day for five days) can reduce the time until resolution of postpartum hypertension [66], especially if hypertension is accompanied by severe edema or related to NSAIDs, although the use of any diuretic in this setting has not been studied extensively [67-70]. (See 'Loop diuretics' below.)

If additional agents are required and the patient is breastfeeding, consult with a pediatrician or other authority. (See 'Drug options during breastfeeding' below.)

Target blood pressure — The initial goal is to maintain blood pressure below 140/90 mmHg until the effects of pregnancy dissipate and blood pressure stabilizes. In patients on antihypertensive therapy, systolic blood pressures ≥140 mmHg or diastolic blood pressures ≥90 mmHg in the 12 hours before discharge were associated with a three-fold increase in risk for readmission because of hypertensive complications compared with those who were discharged normotensive, in one study [71]. (See 'Course' below.)

For patients with a past history or a new diagnosis of chronic hypertension, the blood pressure goal is the same as that for any nonpregnant patient. (See "Overview of hypertension in adults", section on 'Blood pressure goals (targets)'.)

Analgesia — Acetaminophen is the preferred analgesic for postpartum hypertensive patients with mild to moderate pain.

The author believes that NSAIDs can usually be used safely for two to four days in hypertensive patients and in whom blood pressure is monitored closely and is stable or decreasing to the target range. She would use NSAIDs with caution in patients with persistent postpartum hypertension, especially those who are older or salt sensitive or with baseline renal dysfunction. The elevation in blood pressure with NSAIDs is more pronounced in these groups, especially with prolonged NSAID use, such as after a cesarean birth. If acetaminophen alone is ineffective, the risk from NSAIDs needs to be balanced with the risks associated with opioids, which are another alternative. Although the overall risk of increasing blood pressure or causing persistent blood pressure elevation appears to be low with short-term (approximately four days) use, the author has seen such cases and hypertensive crises have been reported in postpartum patients receiving NSAIDs [72-77]. Hypertension associated with NSAID use is likely related to decreased salt excretion, and a brief course of furosemide may be effective in lowering blood pressure in these circumstances. (See "NSAIDs and acetaminophen: Effects on blood pressure and hypertension".)

NSAID use has been studied in the setting of postpartum hypertension in five retrospective studies and five small randomized trials. A meta-analysis of these studies concluded that NSAIDs may be as safe as acetaminophen in patients with hypertension in pregnancy who are followed until discharge (between two and four days postpartum) [26]. Only one trial found NSAIDs to be associated with persistently higher blood pressures compared with acetaminophen in patients followed for 96 hours postdelivery [75]. Based on these data and concerns about the opioid use disorder, the American College of Obstetricians and Gynecologists (ACOG) suggests considering NSAIDs as first-line agents for management of postpartum pain in all individuals, including those with hypertension [78].

However, there are several limitations to these studies: The total number of patients was small, follow-up was very short without clear ascertainment of analgesic drug use after discharge, patients were more likely to have preeclampsia than chronic hypertension, the cumulative dose of the NSAID was not provided, and blood pressure levels at discharge were not available in two trials. The authors of the meta-analysis judged the credibility of evidence to be very low due to the retrospective design of most of the studies, small sample size, and wide confidence intervals. Additional concerns regarding these data relate to generalizability to older patients with longer duration of preexisting chronic hypertension and additional cardiovascular risk factors. For all of these reasons, the author recommends caution in use of NSAIDs in such cases.

Monitoring after discharge — Blood pressure should be followed closely after discharge since blood pressure peaks three to six days postpartum when most patients are at home. Patients should be advised to seek medical attention if they develop severe headaches or if blood pressure increases to severe levels. ACOG suggests daily blood pressure evaluation for 72 hours postpartum and again around 7 to 10 days postpartum, or earlier in patients with symptoms [79,80]. Another approach is to ensure measurement at least once during postpartum days 3 to 5 [81]. Adjunctive home blood pressure monitoring is useful for daily monitoring [82]. Antihypertensive drug management may be performed by physician-guided remote telemonitoring, which may provide better long-term blood pressure control than usual outpatient care [83].

An additional concern in patients discharged on antihypertensive drugs is that they may develop hypotension as their blood pressure returns to the normal baseline level. If prepregnancy blood pressure was normal and the patient is normotensive on medication, it is reasonable to stop the antihypertensive drug after approximately three weeks and monitor blood pressure to assess whether further treatment is indicated. Such patients can be managed or co-managed with their primary care provider.

Course — Hypertension usually resolves spontaneously within a few weeks (average 16±9.5 days) and is almost always gone by 12 weeks postpartum [62,84,85]. However, one small prospective study observed that as many as 50 percent of patients with a history of preeclampsia had hypertension 6 to 12 weeks postpartum [86] and some cases may take as long as six months to resolve [84]. Hypertension that persists beyond six months should be evaluated and treated as in any nonpregnant adult. (See "Overview of hypertension in adults", section on 'Blood pressure goals (targets)'.)

Drug options during breastfeeding — Beta blockers and calcium channel blockers enter breast milk; however, most appear to be safe for the infant [87] and are considered compatible with breastfeeding by experts (see individual drugs in the Lexicomp drug program included with UpToDate or LactMed). It is prudent to consult with the infant's pediatrician before initiating maternal antihypertensive drugs in breastfeeding patients.

Within each class of antihypertensive agents, physicians should select the medication with the lowest transfer into human milk [88]. A brief synopsis is presented below:

●Beta blockers and alpha/beta blockers – Propranolol, metoprolol, and labetalol have the lowest transfer into milk of this class of drug with relative infant doses of less than 2 percent. None have been associated with adverse events in infants.

By contrast, atenolol and acebutolol are more extensively excreted into breast milk, and beta blockade in nursing infants has been reported [89-91]; therefore, other beta blockers are preferable for patients on a high dose of these drugs or who are nursing an infant less than three months of age or a preterm infant.

Because there is little to no published experience with carvedilol or bisoprolol during breastfeeding, other agents are preferred, especially when nursing a newborn or preterm infant.

●Calcium channel blockers – Diltiazem, nifedipine, nicardipine, and verapamil are associated with a relative infant dose of less than 2 percent, which is acceptable.

●ACE inhibitors – These drugs are transferred into milk at very low levels. Captopril and enalapril may be used in lactating patients. However, newborns may be more susceptible to the hemodynamic effects of these drugs, such as hypotension, and sequelae, such as oliguria and seizures. Therefore, we suggest that the hemodynamic status of the infant be considered when deciding whether patients taking these drugs should breastfeed.

There is no information on use of angiotensin II receptor blockers (ARBs) during breastfeeding.

●Diuretics – Theoretically, diuretics may reduce milk volume. Hydrochlorothiazide <50 mg/day is considered safe for the newborn during lactation.

Intense diuresis from a loop diuretic may decrease milk production when lactation is being established, but low doses with more gradual diuresis are less of a concern. The effects of loop diuretics on established lactation have not been studied.

●Methyldopa and hydralazine – Both of these drugs appear to be safe for the newborn. Because maternal depression has been reported following methyldopa administration and postpartum patients are already at risk for postpartum depression, ACOG suggests avoiding use of methyldopa in postpartum patients [11].

OVERVIEW OF ANTIHYPERTENSIVE DRUGS USED IN PREGNANCY

Background — All antihypertensive drugs cross the placenta. There are limited data from large well-designed randomized trials on which to base a strong recommendation for use of one drug over another. Data regarding both comparative efficacy in improving pregnancy outcome and fetal safety are inadequate for almost all antihypertensive drugs. Although adverse fetal and neonatal outcomes have been reported in patients exposed to antihypertensive medications during pregnancy, clear conclusions about the impact of these drugs on pregnancy and the fetus are not possible given the significant methodologic weaknesses and lack of statistical power of available studies [92,93].

Adding to the confusion in this area are data suggesting that offspring of mothers with chronic hypertension, either treated or untreated, are at increased risk for congenital malformations, particularly cardiac malformations, compared with offspring of normotensive mothers. Although it is possible that hypertension increases the risk for congenital heart disease (CHD) and that antihypertensive drugs further increase this risk, it is also possible that hypertension and CHD share similar risk factors.

●In a meta-analysis that evaluated the risk of CHD in offspring of patients with hypertension during pregnancy compared with offspring of those without hypertension, the risk of CHD was approximately 80 percent higher in patients with hypertension (relative risk [RR] 1.8, 95% CI 1.5-2.2) [94].

When the effect of treatment was analyzed, the risk of CHD was 100 percent higher in treated hypertensive patients (RR 2.0, 95% CI 1.5-2.7) and 40 percent higher in untreated hypertensive patients (RR 1.4, 95% CI 1.2-1.7).

The magnitude of effect was generally similar across subtypes of CHD and across the range of antihypertensive therapies; however, data were insufficient to exclude modest differences. Although a positive association was noted in 14 of 15 studies, these results should be interpreted with caution as neither a dose-response relationship between maternal antihypertensive medication and CHD nor some potentially important characteristics of the population (eg, severity of hypertension) could be ascertained.

Choice and safety by drug class — The following drugs are effective antihypertensive agents with an acceptable safety profile in pregnancy. The choice of drug depends on the acuity and severity of hypertension, whether parenteral or oral therapy is appropriate, side effects, and presence of comorbidities (eg, asthma); these factors are discussed below. Additional factors include local practice, drug availability, licensed status (whether the drug is off-label in pregnancy), and cost, which can vary by country.

Response to antihypertensive medication is variable, and generalizations about comparative efficacy in overall or specific hypertensive populations are difficult to make. The most widely used medications (labetalol, hydralazine, nifedipine, methyldopa) have not been examined in comparative effectiveness trials.

Beta blockers — Beta blockers are widely used in pregnancy. Asthma is a common contraindication as bronchospasm may occur [95]. Maternal bradycardia and greater than first-degree heart block are other contraindications.

●Choice of beta blocker

•Labetalol (beta blocker with alpha-blocking activity) is the preferred drug in this class because early studies in experimental models suggested that it may preserve uteroplacental blood flow to a greater extent than nonselective or beta-1 selective blockers.

Labetalol has been associated with maternal hepatotoxicity, which, although rare, is important to recognize as it may be confused with the elevated liver chemistries of preeclampsia with severe features and HELLP syndrome. Most cases are reversible [96], but fatalities have been reported [97].

•Carvedilol is another beta blocker with alpha-blocking activity, but there is less information on outcomes with use in pregnancy [98].

•Metoprolol (beta-1 selective blocker) and pindolol (beta blocker with intrinsic sympathomimetic activity) are considered acceptable alternatives to labetalol based on limited data in pregnant patients [99].

•Atenolol and propranolol are generally avoided. (See 'Selected beta blockers: Atenolol and propranolol' below.)

●Evidence of the safety of beta blockers – Despite the widespread use of labetalol in pregnancy, the safety of beta blockers remains somewhat controversial due to inconsistent reports of preterm birth, fetal growth restriction/small for gestational age infants, perinatal mortality, and neonatal apnea, bradycardia, and hypoglycemia [92,100-103], as well as inconsistent reports of an increased risk for congenital malformations [94,104-108]. Further research is required given the limitations of available data, including inability to analyze data by type of beta blocker; variability in timing of exposure within the first trimester; duration of use; and the fact that most studies did not address differences in indications for beta-blocker therapy (eg, hypertension versus control of heart rate) or recall, recording, publication, and survivor biases.

•In a meta-analysis of 13 population-based case-control or cohort studies examining the risk of congenital malformations associated with first-trimester oral beta-blocker exposure compared with no exposure, there was no overall increase in major congenital malformations (odds ratio [OR] 0.90, 95% CI 0.91-1.10) [104]. Associations with some organ-specific malformations were observed: cardiovascular abnormalities (OR 2.01, 95% CI 1.18-3.42, four studies), cleft lip/palate (OR 3.11, 95% CI 1.79-5.43, two studies), and neural tube defects (OR 3.56, 95% CI 1.19-10.67, two studies).

•In a systematic review specifically examining the risk for congenital heart abnormalities associated with treated and untreated maternal hypertension, beta-blocker therapy was associated with an increased risk compared with no treatment (RR 2.1, 95% CI 1.6-2.7) [94].

•Subsequent studies have reported conflicting results but overall have generally been reassuring that there is no large relative or absolute increase in the risk for overall malformations or cardiac malformations that is independent of measured confounders (eg, hypertension, obesity, diabetes) [105-108]. The International Pregnancy Safety Study (InPreSS) Consortium pooled data from large cohorts drawn from six countries and reported that beta-blocker use was not associated with large increases in the relative and absolute risks for major malformations overall (RR 1.07, 95% CI 0.89-1.30; risk difference per 1000 persons exposed 3.0, 95% CI -6.6 to 12.6) or cardiac malformations (RR 1.12, 95% CI 0.83-1.51; risk difference per 1000 persons exposed 2.1, 95% CI -4.3 to 8.4), the most common class of congenital malformation [107]. Strengths of this study were that medication use was defined based on exposure during the first trimester, the major period of organogenesis; exposure was based on filled prescriptions, which avoided recall bias but did not confirm actual intake of the medication; and the analysis was restricted to females with hypertension, addressing the issue of confounding by this common indication for beta blockers.

Calcium channel blockers — Side effects include headache, lightheadedness, flushing, and dose-dependent peripheral edema. (See "Major side effects and safety of calcium channel blockers".)

●Choice of calcium channel blocker

•Nifedipine, a dihydropyridine calcium channel blocker, is the most commonly used drug in this class in pregnancy. It is widely available in immediate-release (rapid-acting) and extended-release formulations. An intermediate-acting tablet (nifedipine retard) is also available in some countries [109]. We generally prefer to use an intermediate- or extended-release formulation. (See 'Nifedipine' above.)

•Nicardipine is an effective treatment of hypertension in pregnancy, with a good maternal and fetal safety profile [31,48,110-113]. It can be given as a continuous intravenous infusion if prompt treatment of severe hypertension is needed. Oral treatment can be initiated in patients with moderate hypertension (systolic blood pressure 150 to 159 mmHg and/or diastolic blood pressure 100 to 109 mmHg) or after initial acute therapy of severe hypertension. (See 'Treatment of hypertension refractory to first-line acute therapy' above.)

•Although amlodipine is widely used in nonpregnant individuals with hypertension, only sparse data are available on its use in pregnancy [114-116]. The largest report of documented birth outcomes was among 231 Japanese patients, of whom 48 had first-trimester exposure to amlodipine, 54 were exposed to other antihypertensives, and 129 had hypertension but were not exposed to any drug [115]. The rate of fetal morphologic abnormalities was similar in the three groups (range 4.2 to 5.6 percent), suggesting that amlodipine may not be associated with an increased risk of malformations. In another study, the incidence of major congenital anomalies in offspring of women with and without first-trimester amlodipine exposure was 11.4 percent (5 in 44) and 9.0 percent (12 in 134), respectively, and the incidence of multiple anomalies was 2.3 percent (1 in 44) and 2.2 percent (3 in 134), respectively [116]. No specific trend was observed. The adjusted odds ratio for major congenital anomalies with amlodipine versus other antihypertensive exposure was 1.23 (95% CI 0.40-3.72). There is less information on other dihydropyridines (felodipine, nisoldipine, isradipine).

•Nondihydropyridine calcium antagonists, such as verapamil and diltiazem, have been used as well, although most reports in the literature included only a small number of pregnant patients. They slow heart rate and can slow atrioventricular conduction, and thus must be used with caution in patients who are also taking a beta blocker.

●Evidence of safety of calcium channel blockers – Calcium channel blockers have been widely used for tocolysis and acute blood pressure reduction in the second half of pregnancy, but minimal information is available on fetal effects in early pregnancy.

A 2022 network meta-analysis evaluating oral antihypertensives for nonsevere pregnancy hypertension found that no significant increases in preterm birth, cesarean birth, neonatal care unit admission, perinatal death, or small for gestational age infants with calcium channel blockers compared with placebo or other commonly used antihypertensive drugs [56].

Nevertheless, the quality of the safety data is variable and better data are needed to definitively rule out safety issues with all antihypertensives.

Methyldopa — Methyldopa, a centrally acting alpha-2 adrenergic agonist, has been widely used in pregnant patients for several decades and its long-term safety for the fetus has been more extensively documented than other antihypertensive agents [100,117,118]. However, it is only a mild antihypertensive agent and has a slow onset of action (three to six hours). Many patients will not achieve blood pressure goals on this oral agent or are bothered by its sedative effect at high doses. A recent drawback to use is that it is more subject to shortages of drug availability than other drugs as several manufacturers have discontinued production.

Although methyldopa is not widely used outside of pregnancy, it remains useful in this setting, particularly in patients who develop adverse effects or are intolerant of other, more widely used medications. A clinical trial (eg, Control of Hypertension in Pregnancy Study [CHIPS] [28]) that utilized methyldopa demonstrated that pregnant patients treated with this drug may have had better outcomes compared with those treated with labetalol, although these data may be biased by residual confounding [118]. A trial comparing oral administration of methyldopa (1000 mg), labetalol (initial dose 200 mg; maximum total 600 mg), and nifedipine retard (initial dose 10 mg; maximum total dose 30 mg) for treatment of severe hypertension in pregnancy in resource-poor settings found that all three drugs successfully lowered blood pressure, and nifedipine retard resulted in controlled hypertension (systolic blood pressure 120-150 mmHg and diastolic blood pressure 70-100 mmHg) in more patients than methyldopa (84 versus 76 percent) [109]. There were no significant differences in serious adverse events among the groups.

Hydralazine — Intravenous hydralazine, a direct arteriolar vasodilator, has been widely used for many years for treatment of acute severe hypertension in pregnancy and is an acceptable antihypertensive drug in this setting [14]. However, the hypotensive response to intravenous hydralazine is less predictable than that seen with labetalol. Although hydralazine can be taken orally, it causes reflex tachycardia and fluid retention, which limit its usefulness in pregnancy unless combined with a beta blocker.

A meta-analysis demonstrated a slightly increased rate of adverse events with hydralazine compared with labetalol, but the evidence was not sufficient to make a definitive recommendation for one drug over the other [119].

Thiazide diuretics — Thiazides, such as hydrochlorothiazide, and thiazide-like diuretics, such as chlorthalidone or indapamide, have not been associated with an increased risk of fetal anomalies, but obstetric concerns about interference with the physiologic volume expansion of pregnancy have limited their use in pregnant patients.

●Patients not already taking a diuretic – Diuretics should only be initiated in pregnancy for treatment of hypertension when clinically indicated for hypertension associated with volume overload (chronic kidney disease or heart failure), or when other agents have not been successful in achieving blood pressure targets. Plasma volume decreases to a variable degree within the first two weeks of initiating treatment, assuming that drug dose and dietary sodium intake are relatively constant. After the initial two weeks, compensatory stimulation of the renin angiotensin system occurs and plasma volume increases, although usually not back to baseline. The theoretical concern with diuretic use is that this decrease in plasma volume may reduce uteroplacental perfusion, although this has not been well documented. There are no recent studies on the use of diuretics in pregnancy [120-122]. Given their efficacy and widespread use in the nonpregnant hypertensive population, it may be reasonable to study these drugs in pregnancy.

●Patients taking a diuretic – As discussed above, in patients already taking these drugs preconception, we believe that they may be continued in pregnancy [11,123]. (See 'Preconception management of chronic hypertension' above.)

Loop diuretics

●Antepartum hypertension – Loop diuretics are not used for treatment of hypertension during pregnancy. In a meta-analysis of observational studies that assessed cardiac output before and after acute loop diuretic therapy, cardiac output fell by 0.75 L/min (95% CI -1.11 to -0.39), which could result in decreased placental perfusion [124].

●Heart failure – Loop diuretics are the preferred approach to treatment of heart failure with pulmonary congestion during pregnancy. A thiazide diuretic may be added if volume cannot be adequately controlled with a loop diuretic alone (see "Management of heart failure during pregnancy", section on 'Diuretics').

●Postpartum hypertension – Loop diuretics can be effective postpartum when hypertension is accompanied by edema. A meta-analysis of randomized trials found that postpartum use for treatment of hypertension decreased the need for additional antihypertensive medications by 30 percent (RR 0.69, 95% CI 0.50-0.97); however, they did not reduce the need for antihypertensive therapy at the time of hospital discharge and did not reduce the incidence of persistent postpartum hypertension [124]. (See 'Approach to patients with severe versus nonsevere hypertension' above.)

Clonidine — Clonidine has a similar mechanism of action as methyldopa and can be an effective drug for treatment of nonsevere hypertension in pregnancy [125-127]. However, it has bothersome side effects and the possibility of rebound hypertension if it is stopped suddenly, so other agents are preferred.

The author has prescribed clonidine for rare patients in whom methyldopa, labetalol, and nifedipine could not be used. Because clonidine is available as a transdermal patch, it is particularly useful for patients who cannot take an oral antihypertensive drug.

DRUGS TO AVOID IN PREGNANCY

Selected beta blockers: Atenolol and propranolol

●Atenolol (beta-1 selective blocker) has been associated with slightly lower placental and fetal weight at delivery when used early in pregnancy and is generally avoided if an effective drug with a better safety profile is available [26,128,129].

●Propranolol and other nonselective beta blockers are also generally avoided. They may promote uterine irritability since myometrial relaxation of the gravid uterus is a beta-2-adrenergic receptor-mediated process (beta-adrenergic receptor agonists are used for tocolysis).

ACE inhibitors, ARBs, direct renin inhibitors — We do not initiate angiotensin-converting enzyme (ACE) inhibitors, angiotensin II receptor blockers (ARBs), or direct renin inhibitors during pregnancy, and we discontinue them in females planning pregnancy and switch to another agent [130]. (See 'Preconception management of chronic hypertension' above.)

These drugs are associated with significant fetal renal abnormalities when fetal exposure has been in the latter half of pregnancy. An association between first-trimester exposure to ACE inhibitors (and probably ARBs) and cardiovascular and central nervous system malformations that was reported in a small early study has become less convincing after publication of additional analyses of much larger samples that did not confirm the association, although questions of safety remain. (See "Adverse effects of angiotensin converting enzyme inhibitors and receptor blockers in pregnancy".)

Mineralocorticoid receptor antagonists — The use of mineralocorticoid receptor antagonists (MRAs; eg, spironolactone, eplerenone) for treatment of hypertension in pregnancy is generally not recommended. MRAs competitively inhibit aldosterone binding to the mineralocorticoid receptor, which ultimately increases epithelial sodium channel degradation and thus results in reduced sodium reabsorption and reduced potassium excretion. These drugs are diuretics and lower blood pressure, particularly in salt-sensitive hypertension and patients with hyperaldosteronism.

●Spironolactone – Spironolactone, the first-generation MRA, has a very strong antagonistic effect on the mineralocorticoid receptor (MR), however, it also binds to other steroid receptors, such as androgen and progesterone receptors, leading to its well-known side effects, such as gynecomastia and impotence. Eplerenone, a second-generation MRA, has greater selectivity for the MR, which limits these undesirable hormonal side effects. Both drugs are associated with hyperkalemia in patients with impaired kidney function.

Spironolactone crosses the placenta and has never been proven to be safe in pregnancy. The anti-androgenic activity of spironolactone has always been a concern, particularly in male fetuses. Feminization of male rat fetuses has been reported after treatment of pregnant female rats with high doses of spironolactone [131]. A review described one case report of ambiguous genitalia in a human newborn of a mother treated with spironolactone [132] and a few cases of healthy newborns after spironolactone exposure.

●Eplerenone and amiloride – Whether eplerenone, an MRA without anti-androgenic properties introduced approximately 20 years ago, will be safe for human pregnancy is unknown as experience is limited to a few case reports, which did not describe adverse fetal effects [133-135]. The epithelial sodium channel inhibitor amiloride has been used rarely to treat pregnant patients with hyperaldosteronism, Gitelman syndrome, or Liddle's syndrome, and there are sporadic case reports with favorable outcomes [136,137]. We cannot recommend their use at this time because of limited experience.

Nitroprusside — Limited clinical experience (22 pregnancies [138]) and the possibility of fetal cyanide poisoning have restricted the use of nitroprusside in pregnancy. Nitroprusside is an agent of last resort for urgent control of refractory severe hypertension; its use should be limited to a short period of time in an emergency [138,139].

NONPHARMACOLOGIC INTERVENTIONS

Physical activity — We do not advise bed rest for most pregnant patients with hypertension, particularly those with stable chronic hypertension. Restricted activity is disruptive for most patients and can be associated with deconditioning, bone loss, and an increased risk of thromboembolic events [140,141]. Exercise may even have a role in prevention of hypertensive disorders of pregnancy [142], particularly in high-risk patients (eg, gestational diabetes, overweight or obesity) [143].

Reduced activity (including bed rest) for patients with preeclampsia may improve uteroplacental blood flow and prevent exacerbation of hypertension, particularly if blood pressure is not adequately controlled; however, there is no evidence that it significantly improves major maternal or fetal outcomes.

Recommendations for level of activity should be individualized; for example, a patient with stable chronic hypertension early in pregnancy is unlikely to benefit from limited physical activity, while a patient with newly diagnosed preeclampsia in the third trimester may have more stable blood pressure if they limit physical activity while being managed as an outpatient.

No large randomized trials have evaluated the benefits and risks of bed rest in the management of pregnant patients with hypertension of any etiology. A meta-analysis of bed rest during pregnancy for management of hypertension included only four trials with a total of 449 participants [144]. Two trials (145 participants) compared strict bed rest with some rest in the hospital for patients with proteinuric hypertension and did not find any differences in outcome between the groups. The other two trials (304 participants) compared some bed rest in the hospital with routine activity at home for patients with nonproteinuric hypertension and reported some bed rest was associated with a reduced risk of severe hypertension (one trial, 218 participants, relative risk [RR] 0.58, 95% CI 0.38-0.89) and a borderline reduction in risk of preterm birth (one trial, 218 participants, RR 0.53, 95% CI 0.29-0.99).

Postpartum, the potential cardiometabolic health benefits of exercise should be emphasized and is good clinical practice. (See "The benefits and risks of aerobic exercise" and "Exercise in the treatment and prevention of hypertension".)

Diet — A healthy diet without significant salt restriction is generally advised. 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 [145-150]. For patients already on one of these diets, continuation during pregnancy is reasonable. Initiation of extreme salt restriction is discouraged as it may induce low-intravascular volume and there is no convincing evidence to suggest that it helps in the prevention or treatment of hypertension during pregnancy.

DEVELOPMENT OF HYPERTENSION IN NONPREGNANT PATIENTS AFTER HYPERTENSION FIRST PRESENTING IN PREGNANCY — In patients with a history of gestational hypertension, preeclampsia, eclampsia, or HELLP syndrome, at least annual lifelong measurement of blood pressure is important given their increased risk for developing chronic hypertension [58,60,151]. In a population-based study, among primiparous patients in their 20s with versus without a hypertensive disorder of pregnancy, the frequency of hypertension in the first decade postpartum was 14 and 4 percent, respectively [58]. For primiparous patients in their 40s, the rates were 32 and 11 percent, respectively. The increased risk can be observed as soon as the first 12 months after delivery [60]. This risk may be reduced by adherence to a healthy lifestyle (eg, achieving/maintaining a healthy weight, salt restriction, exercise, limited alcohol intake) [59]. (See "Overview of hypertension in adults", section on 'Nonpharmacologic therapy'.)

Patients with preeclampsia with severe features are at particularly high risk of developing sustained hypertension following pregnancy. In a study of 200 such patients referred to the Follow-Up Pre-Eclampsia Outpatient Clinic in Erasmus Medical Center, The Netherlands, and monitored with 24-hour ambulatory blood pressure monitoring (ABPM) at one year postpartum, approximately 42 percent had hypertension (sustained hypertension [15 percent], masked hypertension [18 percent], or white-coat hypertension [10 percent]) with ABPM, and only 24 percent of these patients would have been diagnosed with hypertensive by office measurement of blood pressure alone [152]. However, routine use of ABPM is often not feasible because of expense, lack of access, or lack of insurance coverage. Nevertheless, these data emphasize the need for close attention to traditional cardiovascular risk factors following a hypertensive pregnancy. A detailed discussion of the use of this technique is available separately. (See "Out-of-office blood pressure measurement: Ambulatory and self-measured blood pressure monitoring".)

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" and "Society guideline links: Postpartum care".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5^th to 6^th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10^th to 12^th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

●Basics topics (see "Patient education: Preeclampsia (The Basics)" and "Patient education: High blood pressure and pregnancy (The Basics)")

●Beyond the Basics topics (see "Patient education: Preeclampsia (Beyond the Basics)")

SUMMARY AND RECOMMENDATIONS

●Goals – When hypertension is diagnosed in a pregnant patient, the major issues are establishing a diagnosis (table 1), deciding the blood pressure at which treatment should be initiated and the target blood pressure, and avoiding drugs that may adversely affect the fetus. (See 'Introduction' above and 'Classification of hypertensive disorders in pregnancy' above.)

●Classification – In pregnant patients, we classify hypertension as follows; however, the categories of mild and moderate are not universally recognized (See 'Our approach' above.):

•Mild – Systolic pressure 140 to 149 mmHg and/or diastolic pressure 90 to 99 mmHg

•Moderate – Systolic pressure 150 to 159 mmHg and/or diastolic pressure 100 to 109 mmHg

•Severe – Systolic pressure ≥160 and/or diastolic pressure ≥110 mmHg

●Treatment of severe hypertension in pregnancy – Prompt treatment (within 30 to 60 minutes of diagnosis) of acute severe hypertension is required. Treatment of severe hypertension has a well-established maternal benefit of reduction in stroke risk. (See 'When to initiate antihypertensive therapy in pregnancy' above.)

•For acute therapy, we prefer intravenous labetalol, nicardipine, or hydralazine rather than oral nifedipine, but all are acceptable (algorithm 1 and table 2). (See 'Acute therapy of severe hypertension' above.)

•We try to reduce mean arterial pressure by no more than 25 percent over two hours to achieve initial target blood pressures in the range of 130 to 150 mmHg systolic and 80 to 100 mmHg diastolic. (See 'Target blood pressure' above.)

●Treatment of nonsevere hypertension in pregnancy

•For pregnant patients with chronic nonsevere hypertension (based on medical history or systolic pressure ≥140 mmHg or a diastolic pressure ≥90 mmHg or both on at least two occasions at least 4 hours apart before 20 weeks of gestation), we recommend antihypertensive treatment (Grade 1B). Treatment results in more favorable pregnancy outcomes (reduction in preeclampsia with severe features, medically indicated preterm birth <35 weeks, abruption, or fetal or neonatal death) without increasing the frequency of small for gestational age birth weight. (See 'Patients with nonsevere hypertension (chronic or pregnancy-related)' above and 'Our approach' above.)

•For pregnant patients with new-onset hypertension after 20 weeks of gestation (ie, gestational hypertension or preeclampsia) with systolic pressure 150 to 159 mmHg and/or diastolic pressure 100 to 109 mmHg that persists after multiple inpatient or outpatient blood pressure measurements, we suggest initiating (or increase existing) antihypertensive therapy if delivery is likely to be delayed for more than 24 hours (Grade 2C). (See 'Patients with nonsevere hypertension (chronic or pregnancy-related)' above and 'Our approach' above.)

•For pregnant patients with new-onset hypertension after 20 weeks of gestation (ie, gestational hypertension or preeclampsia) and systolic pressure 140 to 149 and/or diastolic pressure 90 to 99 mmHg that persists after multiple inpatient or outpatient blood pressure measurements, we strongly consider initiating antihypertensive therapy if delivery is likely to be delayed for several days or weeks. This decision is based on individual patient factors and shared decision-making.

We may initiate treatment at even lower levels (systolic pressure 130 to 139 mmHg and/or diastolic pressure 80 to 89 mmHg) in patients with clinical signs and symptoms associated with elevated blood pressure, including evidence of heart failure or cerebrovascular symptoms (eg, chest discomfort, shortness of breath, headache, visual disturbances, confusion) and in younger patients whose baseline blood pressures were low (less than 90/75 mmHg), but we acknowledge that this recommendation is not strongly evidence based. (See 'Patients with nonsevere hypertension (chronic or pregnancy-related)' above and 'Our approach' above.)

•Target blood pressure – In patients in whom antihypertensive therapy was initiated for nonsevere hypertension, our target blood pressure is <140/90 mmHg. (See 'Oral maintenance therapy' above.)

•Drug dosing for oral therapy is shown in the table (table 3). We prefer labetalol or intermediate-acting or extended-release nifedipine. Oral hydralazine may be added if needed to achieve and maintain target blood pressure. Methyldopa is also acceptable, but many patients will not achieve blood pressure goals or are bothered by its sedative effect at high doses. (See 'Oral maintenance therapy' above.)

•Angiotensin-converting enzyme (ACE) inhibitors, angiotensin II receptor blockers (ARBs), and direct renin inhibitors are contraindicated at all stages of pregnancy because of the potential for teratogenesis. (See 'ACE inhibitors, ARBs, direct renin inhibitors' above.)

●Postpartum hypertension – Blood pressure peaks three to six days postpartum. Postpartum hypertension may be due to a variety of causes. (See 'Etiology' above.)

•We suggest antihypertensive therapy for patients with systolic pressure ≥140 mmHg and/or diastolic pressure ≥90 mmHg that persists at time of discharge from the birthing facility (Grade 2C). Oral medications similar to those used in the nonpregnant population can be prescribed (table 3), with modifications if the patient is breastfeeding. Brief furosemide therapy (20 mg orally once or twice per day for five days) is an option, especially if hypertension is accompanied by edema. (See 'Management' above and 'Drug options during breastfeeding' above.)

•When treatment is initiated postpartum, the initial goal is to maintain blood pressure below 140/90 mmHg until the effects of pregnancy dissipate and blood pressure stabilizes, which typically occurs by 6 to 12 weeks postpartum. In patients with a past history or a new diagnosis of chronic hypertension, the blood pressure goal at that point is the same as that for any nonpregnant patient. (See 'Target blood pressure' above and 'Course' above.)

●Postpartum follow-up – Blood pressure should be checked daily for 72 hours postpartum and again no later than 7 to 10 days postpartum. Adjunctive home blood pressure monitoring is useful, if possible. (See 'Monitoring after discharge' above.)

●Discontinuing antihypertensive therapy postpartum – If prepregnancy blood pressure was normal and the patient is normotensive on medication after delivery, stopping or tapering the antihypertensive drugs after approximately three weeks is reasonable. Blood pressure should still be monitored to assess whether further treatment is indicated. (See 'Monitoring after discharge' above.)

●Long-term prognosis – Patients with pregnancy-associated hypertension are at increased risk for developing chronic hypertension and other manifestations of cardiovascular disease and should undergo at least annual lifelong blood pressure measurement. Traditional cardiovascular risk factors, including hyperlipidemia, diabetes, obesity, and sedentary lifestyle, should also be addressed. (See 'Development of hypertension in nonpregnant patients after hypertension first presenting in pregnancy' above.)