CLINICAL OBSTETRICS AND GYNECOLOGY

Volume 60, Number 1, 206–214

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Chronic Hypertension
in Pregnancy:
Diagnosis,
Management, and
Outcomes
NANA-AMA E. ANKUMAH, MD, and BAHA M. SIBAI, MD
Division of Maternal-Fetal Medicine, Department of Obstetrics,
Gynecology, and Reproductive Sciences, McGovern Medical
School, University of Texas Health Science Center at Houston,
Houston, Texas

Abstract: Chronic hypertension affects up to 5% of

pregnancies. Women can be stratified into low-risk or
high-risk chronic hypertension based on baseline
laboratory and diagnostic work-up, comorbid con-
ditions, and outcomes in prior pregnancies. Pregnan-
cies complicated by chronic hypertension are at risk
for increased adverse maternal and neonatal out-
comes including superimposed preeclampsia, fetal
growth restriction, placental abruption, and perinatal
death. Mainstays of management include blood
pressure control, close monitoring for development
of superimposed preeclampsia, serial ultrasound as-
sessment of fetal growth, and antenatal testing after
32 weeks.
Key words: chronic hypertension in pregnancy, super-
imposed preeclampsia, antihypertensives
Correspondence: Nana-Ama E. Ankumah, MD, Divi-
sion of Maternal-Fetal Medicine, Department of Ob-
stetrics, Gynecology, and Reproductive Sciences,
Maternal-Fetal Medicine, University of Texas Health
Science Center at Houston, McGovern Medical
School, 6431 Fannin Street, MSB 3.262, Houston,
TX 77030. E-mail: nana.ama.e.ankumah@uth.tmc.edu
The authors declare that they have nothing to disclose.
Introduction
Chronic hypertension currently affects
up to 5% of pregnancies depending on
the population studied,1 and its preva-
lence has risen over the past decade due
to many factors: delayed childbearing
(B20% of chronic hypertensives); in-
creasing prevalence of obesity (B30%
to 35% of chronic hypertensives); and
increasing number of pregnancies with
significant medical comorbidities such as
pregestational diabetes, lupus, and renal
disease.2,3 It disproportionally affects the
non-Hispanic, black population4; in the
United States in 2013, 3.1% of non-
Hispanic blacks were affected compared
with 1.4% of non-Hispanic whites and
0.9% of Hispanics.5 Chronic hyperten-
sion is a major risk factor for preeclamp-
sia and adverse perinatal outcomes. This
chapter will focus on the diagnosis and

CLINICAL OBSTETRICS AND GYNECOLOGY / VOLUME 60 / NUMBER 1 / MARCH 2017

206 | www.clinicalobgyn.com
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FIGURE 1. Diagnostic criteria of superimposed preeclampsia.
management of chronic hypertension
during pregnancy, associated adverse
perinatal outcomes, and risks in future
pregnancies.
Definitions and Diagnosis
Chronic hypertension in pregnancy is
defined as systolic blood pressure (BP)
Z140 mm Hg and/or diastolic BPZ90
mm Hg documented either before preg-
nancy or before the 20th week of gesta-
tion on at least 2 separate occasions at
least 4 hours apart.1 The diagnosis of
chronic hypertension may prove difficult
during pregnancy, as women of child-
bearing age may not seek regular health
care until pregnancy; thus a chronic
hypertensive presenting for care in the
second trimester may present with nor-
mal BPs given the physiologic decrease in
BP. In these cases, subsequent hyper-
tension in the late second trimester or
third trimester is classified as gestational
hypertension, and the diagnosis of
chronic hypertension may not be con-
firmed until at least 12 weeks postpar-
tum.2
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Chronic Hypertension in Pregnancy 207
BPs in pregnancy are characterized as
either mild (systolic BP, 140 to 159 mm
Hg and/or diastolic BP, 90 to 109 mm
Hg) or severe (systolic BPZ160 and/or
diastolic BPZ110).1 Women with chro-
nic hypertension, but specifically women
with severely elevated BPs, are at in-
creased risk of developing superimposed
preeclampsia, which can be difficult to
differentiate from their primary dis-
ease.2,6,7 Superimposed preeclampsia on
chronic hypertension should be consid-
ered with any of the criteria displayed
in Figure 1, as pregnancy management
and timing of delivery vastly differs from
that of uncomplicated chronic hyper-
tension.
Preconception and Early
Pregnancy Evaluation of
Chronic Hypertension
Ideally, women with chronic hyperten-
sion should be evaluated before concep-
tion with emphasis on determining the
etiology of hypertension, achieving good
BP control, and also achieving control of
comorbid conditions.2,3 The most com-
mon form of chronic hypertension is
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208 Ankumah and Sibai
FIGURE 2. Secondary causes of chronic hypertension.
essential or primary hypertension. How-
ever, in young individuals, women with
BPs that are difficult to control, or
women requiring multiple antihyperten-
sive agents to achieve BP control, a more
thorough investigation should be carried
out to determine potential secondary
causes of hypertension (Fig. 2).2,3 If a
secondary cause is found, the underlying
condition should be treated.
Basic evaluation for pregnant women
with chronic hypertension includes labo-
ratory studies to assess for comorbidities
and for end-organ damage. A hemoglo-
bin A1c should be collected to assess for
pregestational diabetes. A baseline elec-
trocardiogram should be obtained with
attention to the presence of left ventricu-
lar hypertrophy. In women with long-
standing chronic hypertension (Z5 y), an
echocardiogram should be performed to
assess global heart function as well as left
ventricular function.2 Serum creatinine
and proteinuria assessment, either with
a spot urine protein/creatinine ratio or 24
hour urine, should be collected to assess
for renal disease and to serve as a baseline
for comparison later in pregnancy as an
aid in the diagnosis of superimposed
preeclampsia.1,2 The collection of a lipid
profile can also be used to further assess
health risk, though treatment of dyslipi-
demia during pregnancy is currently not
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recommended, as there is concern about
the safety profile of statins.2 A detailed
history and physical should be elicited
with special attention to current antihy-
pertensive therapies, prior surgery, and
outcomes in prior pregnancies.
Maternal and Perinatal
Outcomes Associated With
Chronic Hypertension
Results of the preliminary work-up can
aid the clinician in classifying hyperten-
sive women into low-risk and high-risk.
Although low-risk women tend to have
excellent pregnancy outcomes, high-risk
women are at increased risk for poor
maternal and neonatal outcomes. High-
risk women should be counseled for
increased frequency of outpatient visits
for BP monitoring and high probability
for hospitalizations during the preg-
nancy.2
Women with chronic hypertension
have increased risk of adverse maternal
outcomes compared with the general
obstetric population. Superimposed pre-
eclampsia develops in B15% in low-risk
women and upwards of 30% in high-risk
women.2,8 The risk of developing super-
imposed preeclampsia increases with the
presence of baseline proteinuria9 and

TABLE 1. Rate of Adverse Maternal and
Perinatal Outcomes by Risk
Group
Low-Risk High-Risk
CHTN CHTN
Adverse Outcome (rate %) (rate %)
Superimposed 10-15 25-50
preeclampsia
Development of severe 7-10 20-30
hypertension
Preterm delivery 7-10 20-50
Placental abruption 1-2 15-30
Perinatal death <1 3-15
Renal failure/dialysis <1 1-2
Retinal injury/stroke <1 <1
CHTN indicates chronic hypertension.
BPsZ140 mm Hg and systolic and
Z90 mm Hg diastolic, specifically with
5 mm Hg increases in diastolic BPs, be-
fore 20 weeks gestation.6 The risk of
placental abruption is also increased
among women with chronic hyperten-
sion, especially when in association with
uncontrolled hypertension and fetal
growth restriction.1,2,8 Placental abrupt-
ion in the general obstetric population
occurs at a rate of 1%4,8 and at B1.5% in
women with mildly elevated BPs.4,6,8
However, in the setting of superimposed
preeclampsia, the rate of placental
abruption increases to 3%.10 In addition
to preeclampsia and abruption, women
with mild hypertension are at increased
risk for progression to severe hyperten-
sion with the potential for infrequent life-
threatening maternal complications such
as pulmonary edema, acute renal failure,
and stroke.2
Aside from the mother, chronic hyper-
tension also adversely affects the fetus
and neonate. A recent meta-analysis of 22
trials of women with chronic hyperten-
sion demonstrated a 4% incidence of
perinatal death, which translates to a
4-fold increase.11 This risk is further
increased in the presence of comorbid
conditions, especially collagen vascular
disorders and renal disease.12 Fetal
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Chronic Hypertension in Pregnancy 209
growth restriction is also increased in this
cohort.2,6 The etiology of fetal growth
restriction is multifactorial: aggressive
treatment of hypertension may lead to
decreased uteroplacental perfusion,13
while also severe hypertension can
lead to vasoconstriction and decreased
uteroplacental perfusion apart from
treatment.14 Also, women with severe
hypertension are more likely to require
aggressive antihypertensive treatment,
which may potentiate the increased risk
of fetal growth restriction. Chronic hy-
pertensives are also most likely to require
an indicated preterm delivery, expos-
ing the neonate to the morbidity of
prematurity.6 Table 1 compares the risk
of adverse maternal and perinatal out-
comes between women with low-risk
chronic hypertension versus those who
are high-risk.
Treatment of Elevated Blood
Pressures in Pregnancy
Treatment of hypertension in the general
adult population is based on the premise
that long-standing hypertension is asso-
ciated with adverse health outcomes such
as renal disease, myocardial infarction,
and stroke.15 Long-term BP control has
been shown to decrease these risks.15
However, pregnancy is a relatively short
interval, and therefore, treatment in this
small window may expose the fetus to
risk without conferring much benefit to
the mother.2 There is general consensus
that women with severe elevations in BP
should be treated with antihypertensive
therapy, as severe BPs put the mother at
risk for hemorrhagic stroke and other
end-organ damage.1 However, there was
no consensus on thresholds for treatment
of mildly elevated BPs in pregnancy.1,2
The Control of Hypertension in Preg-
nancy Study (CHIPS) is the largest
randomized trial comparing tight control
(<85 mm Hg diastolic) versus less-tight
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210 Ankumah and Sibai

TABLE 2. Antihypertensive Agents Used in Pregnancy

Mechanism of
Name Action Dosing Side Effects
Maintenance antihypertensive agents
Labetalol* Nonselective 200-2400 mg orally Bronchospasm
b-blocker divided into Do not use in congestive heart failure
2-3 times/day
dosing
Nifedipine- Calcium 30-120 mg orally Headache
extended channel daily Flushing
release* blocker Reflex tachycardia
Lower extremity edema
Methyldopa a-2 receptor 500-3000 mg orally Transient increase in liver enzymes
agonist divided into
2-3 times/day
dosing
Thiazides Diuretic Depends on agent None known
Metoprolol b-blocker 50-200 mg orally Bronchospasm
extended release daily Do not use in congestive heart failure
Hydralazine Peripheral 40-300 mg orally Palpitations
vasodilator divided into Reflex tachycardia
3-4 times/day
dosing
Furosemide Loop diuretic 20-80 mg orally Electrolyte imbalance
divided into
1-2 times/day
dosing
Acute antihypertensive agents
Labetalol Nonselective 20 mg IV, then Bronchospasm
b-blocker 40 mg IV, then Do not use in congestive heart failure
80 mg IV every
10 min, max
dose 300 mg IV
Hydralazine Peripheral 5-10 mg IV every Caution—multiple doses may cause
vasodilator 20-30 min profound delayed hypotension
Nifedipine Calcium 10-20 mg orally Headache
immediate channel every 20 min Flushing
release blocker for 3 doses Reflex tachycardia

*First-line maintenance antihypertensive agents in pregnancy.

IV indicates intravenous.

control (<100 mm Hg systolic) of women
with both chronic and gestational hyper-
tension.16 Outcomes investigated were
the development of a composite primary
outcome of pregnancy loss or high-level
neonatal care during the first 28 days
of neonatal life, and secondary outcomes
included superimposed preeclampsia,
fetal growth restriction, placental abrupt-
ion, preterm birth, and antenatal hospi-
talization. There was no significant
difference between groups in rate of
either the primary outcome (30.7% vs.
31.4%) or preeclampsia (27% vs. 30%).
Among the subgroup of 736 women with
chronic hypertension (371 randomized to
less-tight group and 365 to tight-control
group), there was no significant differ-
ence between groups in rate of either the
primary outcome (28.9% vs. 30.6%) or in
the rates of secondary maternal outcome
(2.2% vs. 2.7%), although the rate of
progression to severe hypertension was
significantly higher in the less-tight

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 Chronic Hypertension in Pregnancy 211

FIGURE 3. Algorithm for care of women with chronic hypertension.

control group (43.1% vs. 26.4%; odds
ratio, 0.47, 95% confidence interval,
0.34-0.65). As there is no current evidence
that tight control of BPs during preg-
nancy improve maternal or perinatal out-
comes, goals for antihypertensive therapy
in low-risk chronic hypertensives is 120 to
160 mm Hg systolic and 80 to 105 mm Hg
diastolic.1 We call for caution in high-risk
women with evidence of end-organ dam-
age for tighter control of BPs, with goals
<140 mm Hg systolic and <90 mm Hg
diastolic. For women already on antihy-
pertensive therapy at the initiation of
prenatal care with BPs less than or at
the lower end of goal ranges, it is reason-
able to discontinue antihypertensive ther-
apy and monitor BPs, restarting if BPs
exceed the aforementioned thresholds.1,2
For women requiring antihypertensive
in pregnancy, first-line oral agents in-
clude labetalol, a nonselective b-blocker
and nifedipine, a calcium channel block-
er.1 (Table 2). Labetalol should be used
with caution in asthmatics as it can cause
bronchospasm, and should be avoided in
patients with congestive heart failure.1–3
Nifedipine, a calcium channel blocker

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212 Ankumah and Sibai
can also be used in its extended release
form for BP control.1–3 Methyldopa, an
a-2 receptor agonist, has a long safety
profile in pregnancy, but may be less
effective than labetalol and nifedipine in
preventing severe hypertension.7 Thia-
zides are considered second-line agents
in the treatment of chronic hypertension
in pregnancy.1,2 Angiotensin-converting
enzyme inhibitors and angiotensin II
receptor blockers are contraindicated in
pregnancy given their association with
adverse fetal renal and craniofacial de-
fects.1–3 For acute, severe exacerbations
in BPs exceeding 160 mm Hg systolic or
110 mm Hg diastolic, first-line agents
include intravenous labetalol, intrave-
nous hydralazine, or immediate release
oral nifedipine1,2 (Table 2).
Management of Low-Risk
Chronic Hypertension
After the initial baseline work-up detailed
earlier, priorities during pregnancy are
BP control (<160 mm Hg systolic and
<105 mm Hg diastolic) and monitoring
for signs and symptoms of superimposed
preeclampsia. Women should be coun-
seled to report symptoms of preeclampsia
promptly and advised to avoid tobacco
and alcohol use, as this can exacerbate
risks for fetal growth restriction and
placental abruption. Women may be
prescribed BP cuffs and made to perform
BPs logs daily. Depending on BP control,
clinic visits may occur every 3 weeks until
28 to 30 weeks, every 2 weeks until 36
weeks, and then weekly thereafter, with
more frequent visits if BPs are not well
controlled. One may consider an early 1
hour glucose challenge test, especially in
the setting of obesity, as recent investiga-
tions have shown increased rates of gesta-
tional diabetes among women with
chronic hypertension.17
On the fetal side, women should be
offered screening for aneuploidy in the
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first trimester with anatomy ultrasound
to screen for fetal anomalies in the second
trimester around 18 to 22 weeks. Serial
growth ultrasounds should commence at
34 weeks, and earlier if there are sus-
pected growth abnormalities from the
anatomy ultrasound or from in-office
fundal heights. If fetal growth restriction
is identified, weekly antenatal testing and
umbilical artery Doppler should be per-
formed starting at the time of diagnosis.
If there are growth abnormalities or other
indications for antenatal testing, weekly
antenatal testing in the form of biophys-
ical profile or nonstress test should begin
at 34 weeks, and women should be
educated on daily kick counts given
increased risk of intrauterine fetal de-
mise. Delivery should occur at 38 to 39
weeks if there are no other indications for
delivery arise (Fig. 3).
Management of High-Risk
Chronic Hypertension
Management of high-risk chronic hyper-
tension involves more intensive follow-up
given the increased risk in adverse mater-
nal and perinatal outcomes and risk of
further organ deterioration. In-patient
initial evaluation may prove safest and
expedite the completion of all necessary
preliminary evaluations. BPs should be
maintained <140 mm Hg and <90 mm
Hg diastolic for organ protection. Wom-
en should be offered aneuploidy screen-
ing in the first trimester and anatomy
ultrasound in the second trimester, as
well as early 1 hour glucose challenge test
to be repeated in the second trimester if
passed. These women should have fre-
quent antenatal evaluation and also be
educated on the symptoms of superim-
posed preeclampsia. Multidisciplinary
coordination may be necessary given
coexisting medical conditions.
More rigorous fetal evaluation is nec-
essary for this cohort, with serial growth

ultrasounds starting at 28 weeks every 3
weeks, and sooner if concerns for growth
restriction. Weekly antenatal testing in
the form of biophysical profile or non-
stress test should commence at 28-30
weeks gestation until delivery, which
should occur by 37 weeks gestation.
Clinicians should have a low threshold
for hospitalization in these women given
their higher risk of adverse outcomes and
organ deterioration.
Postpartum Management of
Chronic Hypertension
BP control is important with both low-
risk and high-risk chronic hypertension.
As there are not current trials on post-
partum BP goals in women with chronic
hypertension, the current recommen-
dation is <150 mm Hg systolic and
<100 mm Hg diastolic.1 When oral ther-
apy is needed to control BPs, women may
be able to resume BP medications before
pregnancy. Diabetics or women with
cardiomyopathy may benefit from use
of angiotensin-converting enzyme inhib-
itors. If an angiotensin-converting en-
zyme inhibitor is to be used captopril
and enalapril has been studied most in
pregnancy and is compatible with breast-
feeding.1,18 There is little information on
the safety profile of angiotensin II recep-
tor blockers in breastfeeding, and their
use in breastfeeding should currently be
avoided.18 When b-blockers are used,
labetalol and propranolol have lower
concentrations in the breast-milk than
metoprolol and atenolol.18 Diuretics are
in low concentration in the breast-milk
and probably safe based on limited data,
but potentially may decrease milk sup-
ply.18 Nifedipine is compatible with
breastfeeding,18 and is an excellent drug
for women with superimposed pree-
clampsia given its protective renal effects.
Women with high-risk hypertension
should be monitored closely for the de-
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Chronic Hypertension in Pregnancy 213
velopment of serious complications such
as pulmonary edema, congestive heart
failure, and renal failure. Women are at
even higher risk for development of these
complications if they developed super-
imposed preeclampsia, placental abrupt-
ion, or already have end-organ damage.
BP control is of utmost importance in
these women to avoid more serious se-
quelae.
Prognosis in Future
Pregnancies
Prognosis in future pregnancies is good
for low-risk chronic hypertensives. Even
with the development of preeclampsia in
a prior pregnancy, the risk of developing
superimposed preeclampsia in a future
pregnancy may not be increased, though
the risk of an indicated preterm delivery
is increased.19 Advancing maternal age
(Z40 y) and adverse pregnancy outcome
occurring <34 weeks gestation in the
previous pregnancy does increase risk of
adverse pregnancy outcomes in future
pregnancies. In women with high-risk
chronic hypertension, their risk in future
pregnancies is largely dependent on con-
trol of BP as well as status of their
comorbid conditions.
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