Chronic Hypertension
BS. Nguyễn Hồng Anh
In reproductive-aged women, the prevalence o hypertension
approximates 6 percent (Centers or Disease Control and Prevention, 2017). Tus, not surprisingly, chronic hypertension
is one o the most common serious complications encountered during pregnancy. In one study o more than 56 million births, the incidence was 1.8 percent (Bateman, 2012).
Chronic hypertension complicated 2.3 percent o pregnancies
in data rom the Medicaid Analytic Extract (Bateman, 2015).
Despite an increasing prevalence rom 1970 to 2010, optimal
management has not been well studied (Ananth, 2019).
Chronic hypertension usually improves during early pregnancy. Tis is ollowed by variable behavior later in pregnancy
and may include development o superimposed preeclampsia.
Te latter carries signicant risks or maternal and perinatal
morbidity and mortality.
GENERAL CONSIDERATIONS
Blood pressure is a polygenic biological variant that diers
between populations. Numerous epigenetic actors also inuence penetrance dierences between individuals. Moreover,
clinical eatures such as increasing age and weight correlate positively with rising pressures. Last, resting blood pressure measurements do not reect daily activities. Tereore, adults have
a broad range o normal blood pressure values, which makes
dening hypertension difcult.
■ Definition and Classification
Chronic hypertension would logically be dened as some level
o sustained resting blood pressure that is associated with acute
or long-term adverse eects. Most consider 140/90 mm Hg
as the upper limit o normal. In the United States, these values were derived primarily rom lie insurance actuarial tables
constructed using data rom white adult males. Tese “norms”
disregard ethnicity, gender, and other covariants. Te importance o race is emphasized by Kotchen (2018), who cites
the incidence o hypertension—dened as blood pressure
>140/90 mm Hg—to be 34 percent in blacks, 29 percent in
whites, and 21 percent in Mexican Americans.
For many years, the Joint National Committee promulgated guidelines or diagnosis, classication, and management o chronic hypertension. Recently, a coalition led by
the American College o Cardiology and the American Heart
Association published criteria or the diagnosis o hypertension
(Table 53-1) (Whelton, 2018)
TABLE 53-1. Criteria for Diagnosis of Hypertension
■ Treatment and Benefits for
Nonpregnant Adults
Chronic hypertension accounts or nearly 15 percent o deaths
worldwide (Kotchen, 2018). Long term, hypertension raises
substantively the risk o cardiovascular disease, coronary heart
disease, congestive heart ailure, stroke, renal ailure, peripheral arterial disease, and mortality. Tese risks decline with
treatment o otherwise normal adults who have sustained
hypertension.
Based on these benets, current guidelines recommend antihypertensive therapy or stage 1 hypertension in nonpregnant
adults with risk actors or current or uture cardiovascular disease.
However, given the dierent diagnostic criteria in pregnancy (see
able 53-1), the best management or women being treated and
contemplating pregnancy, or those undergoing treatment who
become pregnant, or or those rst identied to have chronic
hypertension during pregnancy is unknown (American College
o Obstetricians and Gynecologists, 2018a; August, 2015). In
these women, the benets and saety o instituting antihypertensive therapy are less clear, as subsequently discussed.
■ Preconceptional Counseling
Women with chronic hypertension ideally undergo counseling beore pregnancy (American College o Obstetricians and
Gynecologists, 2018b). Initial questions ascertain hypertension duration, degree o blood pressure control, and current
therapy. Home measurement devices are checked or accuracy.
General health, daily activities, and dietary habits also are
assessed (Table 53-2). Women who require multiple medications or control or who have poorly controlled pressures carry
greater risk or adverse pregnancy outcomes. Patient counseling
should disclose maternal and etal risks, which are detailed in
later sections (pp. 946 and 948).
For hypertensive women with disease exceeding 5 years or
with comorbid diabetes, cardiovascular and renal unction are
assessed (August, 2015; Chahine, 2019). Renal unction is evaluated by serum creatinine measurement and urine spot protein/
creatinine ratio measurement. I the ratio is abnormally high
(>0.3), proteinuria can be urther quantied with a 24-hour
urine collection (Kuper, 2016; Morgan, 2016a).
Women with evidence o organ dysunction or those with
prior adverse events such as a stroke, myocardial inarction,
arrhythmias, or ventricular ailure carry markedly higher risks
or a recurrence or worsening dysunction during pregnancy.
Specic preconceptional guidance or these conditions is
ound in Chapters 63 (p. 1132) and 52 (p. 918), respectively.
Although poorly controlled hypertension is considered a contraindication or pregnancy by some, there is no consensus.
Women who maintain persistent systolic pressures ≥160 mm
Hg or diastolic pressures ≥110 mm Hg despite therapy; require
multiple antihypertensive agents; have a serum creatinine level
>2 mg/dL; or have a history o prior stroke, myocardial inarction, or cardiac ailure must be counseled regarding the marked
risks to themselves and to their etus. Tese are described in the
next sections.
PREGNANCY CONSIDERATIONS
■ Diagnosis and Evaluation
Chronic hypertension is diagnosed i it precedes pregnancy or
i it is identied beore 20 weeks’ gestation. Prior to this gestational age, preeclampsia is rarely seen (Chap 40, p. 690). Te
American College o Obstetricians and Gynecologists (2018a,
2020) denes hypertension as a systolic pressure ≥140 mm Hg or
a diastolic pressure ≥90 mm Hg (see able 53-1). In suspected
TABLE 53-2. Lifestyle Modifications for Hypertensive Patients
Weight reduction: BMI ≤25 kg/m2
Consume a dietary pattern that emphasizes intake of vegetables, fruits, and whole grains; includes low-fat dairy products,
poultry, fish, legumes, nontropical vegetable oils, and nuts; and limits sweets and red meats. Examples are DASH, USDA
Food Pattern, or the AHA Diet
Lower sodium intake: consume no more than 2400 mg/d; 1500 mg/d desirable
Engage in aerobic physical activity three to four sessions per week, lasting on average 40 minutes per session, and involving
moderate- to vigorous-intensity physical activity
Moderation of alcohol consumption: ≤1 drink daily (none when pregnant)
AHA = American Heart Association; DASH = Dietary Approaches to Stop Hypertension; USDA = United States Department
of Agriculture.
Summarized from Kotchen, 2018; Whelton, 2018.
cases o “white-coat” hypertension, serial ambulatory monitoring can be considered. In some women without overt chronic
hypertension, a history o repeated pregnancies complicated by
gestational hypertension, with or without preeclampsia, may be
elicited. Either is a risk actor or latent chronic hypertension.
Tis is especially true or prior preeclampsia and particularly or
early-onset preeclampsia (van Eerden, 2018). In many ways,
gestational hypertension is analogous to gestational diabetes.
Women with the ormer have a chronic hypertensive diathesis, in
which heredity and epigenetics play a major role.
Although uncommon, secondary causes o hypertension are
always a possibility in aected women. Tus, chronic renal disease, obstructive sleep apnea, connective tissue disease, primary
aldosteronism, Cushing syndrome, pheochromocytoma, and
myriad other causes are considered during evaluation (American
College o Obstetricians and Gynecologists, 2018a). Tat said,
most pregnant women with antecedent hypertension will have
otherwise uncomplicated disease. Te hypertensive disorders that
uniquely complicate pregnancy are discussed in Chapter 40.
■ Risk Factors
Several actors increase the likelihood that pregnant women
will have chronic hypertension. Tree o those most requently
cited are ethnicity, obesity, and diabetes. As previously noted,
black women are more commonly aected. Related to this,
hundreds o blood pressure–related phenotypes and genomic
regions have been identied (Ward, 2015). Obesity may raise
the prevalence o chronic hypertension tenold (Chap. 51, p.
904). In addition, obese women are more likely to develop
superimposed preeclampsia (Ornaghi, 2018).
Te metabolic syndrome is a clinical cluster that includes
hypertension, high blood sugar, excess at at the waist, and abnormal cholesterol or triglyceride levels. Tis constellation is a risk
marker or superimposed preeclampsia and or persistent postpartum hypertension (Jeyabalan, 2015). Diabetes is also prevalent in
chronically hypertensive women, and its interplay with obesity
and preeclampsia is prominent (Leon, 2016). Te most requent
comorbidities associated with chronic hypertension are pregestational diabetes—6.6 percent, thyroid disorders—4.1 percent, and
collagen vascular disease—0.6 percent (Bateman, 2012).
■ Physiological Effects of Chronic Hypertension
Blood pressure decreases in the rst trimester due to a 30-percent
drop in systemic vascular resistance. In most women with chronic
hypertension, this decline is ollowed by a rise in blood pressure
during the third trimester (Fig. 53-1). Women with chronic
hypertension have persistently elevated vascular resistance and
possibly reduced intravascular volume expansion (ihtonen,
2007). Moreover, in women with superimposed preeclampsia,
arterial mechanical properties are most marked (Hibbard, 2015).
ADVERSE PREGNANCY EFFECTS
Chronic hypertension is associated with adverse maternal and
perinatal outcomes listed in Table 53-3. Rates o these complications positively correlate with the severity and duration o
prepregnancy hypertension. Elevated blood pressure dened by
criteria in able 53-1 may herald adverse outcomes similar to
those in women with chronic hypertension dened by criteria o
the American College o Obstetricians and Gynecologists (Keene,
2019; Sutton, 2018). Development o superimposed preeclampsia, particularly early-onset disease, is especially dangerous.
■ Maternal Morbidity and Mortality
Most women with satisactorily controlled hypertension and no
end-organ damage will do well in pregnancy. Complications
are more likely with severe baseline hypertension and documented end-organ damage, especially ventricular hypertrophy
and hypertensive glomerulosclerosis (Ambia, 2018, 2019; Morgan, 2016b). Women with chronic hypertension have higher
rates o stroke, pulmonary edema, and renal ailure (Gilbert,
2007; Zokie, 2018). Tese observations were veried in the
report rom the Nationwide Patient Sample (Bateman, 2012).
140
120
Blood pressure (mm Hg)
100
80
60
160
40
10 15 20 25 30 35 40
Gestational age (weeks)
Chronic hypertension
Normal pregnancy
FIGURE 53-1 Mean systolic and diastolic blood pressures across
pregnancy in 107 untreated chronically hypertensive women
(yellow) compared with blood pressures across pregnancy in 4589
healthy nulliparas (blue). (Data from August, 2015; Levine, 1997;
Sibai, 1990.)
TABLE 53-3. Some Adverse Effects of Chronic
Hypertension on Maternal and
Perinatal Outcomes
Maternal Perinatal
Superimposed preeclampsia Stillbirth
HELLP syndrome Fetal-growth restriction
Placental abruption Preterm delivery
Pulmonary edema Neonatal death
Stroke Neonatal morbidity
Acute kidney injury Congenital anomalies
Heart failure
Hypertensive cardiomyopathy
Myocardial infarction
Maternal death
HELLP = hemolysis, elevated liver enzyme levels, low
platelet count.
In this study, hypertension complications included pulmonary
edema—1.5 per 1000, stroke—2.7 per 1000, mechanical ventilation—3.8 per 1000, acute kidney injury—5.9 per 1000,
and maternal mortality—0.4 per 1000. In another report,
the maternal mortality rate was greater in women with severe
hypertension (Akbar, 2019). Peripartum cardiomyopathy is
another associated risk (Cunningham, 2019).
Dangerous blood pressure elevation can develop with
chronic hypertension. Systolic pressure ≥160 mm Hg or
diastolic pressure ≥110 mm Hg will rapidly cause renal or
cardiopulmonary dysunction or cerebral hemorrhage (Clark,
2012). In addition to hypertensive heart ailure mentioned
above, coronary artery and aortic dissection have been described
(Faden, 2016; Weissman-Brenner, 2004). With superimposed
preeclampsia or eclampsia, the maternal prognosis is poor
unless the pregnancy is ended (Becker, 2018). Placental abruption is a common and serious complication (p. 946).
Chronic hypertension is associated with a veold higher risk
or maternal death (Gilbert, 2007). In the United States rom
2011 to 2013, hypertensive disorders, including chronic hypertension and preeclampsia syndrome, accounted or 7.4 percent
o 2009 pregnancy-related deaths (Creanga, 2017). Undoubtedly related were other causes o death such as cardiovascular conditions—15.5 percent, cerebrovascular accidents—6.6
percent, and cardiomyopathy—11 percent. Moodley (2007)
reported similar ndings in 3406 maternal deaths rom South
Arica.
■ Superimposed Preeclampsia
Te reported incidence o superimposed preeclampsia varies rom 20 to 50 percent because it is not precisely dened
(American College o Obstetricians and Gynecologists, 2018a,
2020; Bramham, 2016; Moussa, 2017). In a Maternal-Fetal
Medicine Units Network trial, superimposed preeclampsia was
diagnosed in 25 percent o hypertensive gravidas (Caritis,
1998). August and colleagues (2015) hypothesize that this
predilection may stem rom similar genetic, biochemical, and
metabolic abnormalities.
Te risk or superimposed preeclampsia positively correlates
with the severity o baseline hypertension and the need or
antihypertensive therapy (Ankumah, 2014; Morgan, 2016a).
Preliminary observations indicate that pregnant women with
initial blood pressures ≥130/80 mm Hg early in pregnancy
have excessive rates o preeclampsia (Greiner, 2020; Keene,
2019; Roman, 2020). Moreover, compared with women who
do not develop preeclampsia, these pressures nadir earlier in
gestation (Fig. 53-2) (Morgan, 2016a). Te preeclampsia risk is
even greater i end-organ damage, such as baseline proteinuria,
is present.
Prediction
Tus ar, individual predictive tests or superimposed preeclampsia have been disappointing (Conde-Agudelo, 2015;
Correa, 2016). First-trimester serum markers used or aneuploidy screening are one group (Chap. 17, p. 338). O these,
inhibin A levels are reduced in patients destined to develop
preeclampsia, but its low sensitivity makes it clinically
unuseul (Sibai, 2008; Zeeman, 2003). Similarly, maternal
serum pregnancy-associated plasma protein-A (PAPP-A) levels
are decreased in the rst trimester o pregnancies that are later
complicated by preeclampsia (an, 2018). O angiogenic and
antiangiogenic actors, low plasma levels o placental growth
actor (PlGF) and high levels o soluble ms-like tyrosine
kinase-1 (sFlt-1) have been associated with superimposed
preeclampsia development (Binder 2020; Nzelu, 2020). Last,
the umbilical artery pulsatility index appears to be elevated
in the rst trimester o these pregnancies (O’Gorman, 2016).
Combining all these actors may be useul in predicting superimposed preeclampsia (O’Gorman, 2016; Stepan, 2020).
Prevention
rials using various medications to prevent preeclampsia in
women with chronic hypertension show little or no benet.
Low-dose aspirin has been evaluated most requently (Mol,
2016; Sta, 2015). Te U.S. Preventive Services ask Force
concluded with “moderate certainty” that treatment with lowdose aspirin or chronically hypertensive women at high risk
or preeclampsia is benecial (Henderson, 2014). Te American College o Obstetricians and Gynecologists (2018a) subsequently recommended initiating 81 mg between 12 and
28 weeks’ gestation and continuing therapy until delivery or
these at-risk gravidas.
Antioxidants to prevent preeclampsia have been studied.
Spinnato and coworkers (2007) randomly assigned 311 women
with chronic hypertension to treatment with vitamins C and E
or with a placebo. A similar number in both groups developed
preeclampsia—17 versus 20 percent, respectively.
Placental Abruption
Chronic hypertension increases the risk two- to threeold or
premature placental separation. Tis event’s harms are detailed
in Chapter 43 (p. 753). Te general obstetrical population risk
is 1 abruption in 200 to 300 pregnancies, and in women with
90
35
Mean arterial pressure (mm Hg)
40
95
100
105
100
115
Preeclampsia
No preeclampsia
Gestational age (weeks)
0 5 10 15 20 25 30
FIGURE 53-2 Blood pressure trends in treated, chronically hypertensive women with and without superimposed preeclampsia.
Mean maternal pressures (MAPs) at entry (p = 0.002) and throughout gestation (p <0.001) are significantly different for each group.
MAP nadir at 23.3 weeks (95% CI, 22.5–24.1) for superimposed preeclampsia versus 26.4 weeks (95% CI, 22.5–27.6) for those without
preeclampsia is significant (3.1 weeks, 95% CI, 2.3–4.3).948
Section 12
Medical and Surgical Complications
chronic hypertension, this rises to 1 in 60 to 120 pregnancies
(Ankumah, 2014; Cruz, 2011; Magee, 2015). Most abruptions
aect women with worsening hypertension or superimposed
preeclampsia. Vigil-De Gracia and associates (2004) reported
an 8.4-percent risk in women with severe hypertension.
■ Perinatal Morbidity and Mortality
Rates o almost all adverse perinatal outcomes are greater in
women with chronic hypertension than in normotensive gravidas. Tose who develop preeclampsia have substantially higher
adverse outcome rates. As shown in Figure 53-3, adverse outcome rates rise incrementally with increasing blood pressures
(Ankumah, 2014). Tere is evidence to suggest that chronic
hypertension—treated or untreated—is associated with congenital anomalies (Battarbee, 2020). Data rom untreated
women help tease away drug eects on organogenesis. Bateman
and coworkers (2015) ound an odds ratio o 1.5 or cardiac
deects. A systematic review noted a comparable risk ratio o
1.4 (Ramakrishnan, 2015). From one large birth deect study,
ve cases o etal esophageal atresia were ound in those with
untreated hypertension and yielded an adjusted odds ratio o
3.2 (van Gelder, 2015).
Te stillbirth requency with chronic hypertension is substantively greater, and common etiologies include superimposed
severe preeclampsia, abruption, and etal-growth restriction.
Rates range rom 15 to 24 deaths per 1000 births (Ahmad,
2012; Ankumah, 2014; Bateman, 2012). Low-birthweight neonates also are common and result rom etal-growth restriction,
indicated preterm delivery, or both (see Fig. 53-3).
Te incidence o etal-growth restriction averages 20 percent. Zetterström and colleagues (2006) reported a 2.5-old risk
or etal-growth restriction in 2754 chronically hypertensive
Swedish women compared with the risk in normotensive gravidas. Another study o 1609 Dutch nulliparas showed a 1.3-old
greater risk (Broekhuijsen, 2012). As with other complications,
etal-growth dysunction is more likely in those who develop
superimposed preeclampsia. In one study, the incidence o
growth-restricted etuses born to women with superimposed
preeclampsia was almost 50 percent compared with only 21 percent in chronically hypertensive women without preeclampsia
(Chappell, 2008). Last, women with chronic hypertension
severe enough to warrant treatment had an 11-percent incidence o etal-growth restriction sufciently severe to yield
birthweights ≤3rd percentile (Morgan, 2016a). Tus, neonates born to these women have a correspondingly high rate o
intensive-care unit (ICU) admission.
All o these adverse perinatal eects o chronic hypertension contribute to the greater perinatal mortality rate, which
is two- to ourold higher than the rate in nonaected gravidas
(American College o Obstetricians and Gynecologists, 2018a).
Stratied by severity, the perinatal death rate was 31 per 1000
births in those with mild hypertension, 72 per 1000 births
with moderate disease, and 100 per 1000 births in women with
severe chronic hypertension (Ankumah, 2014). In a study rom
Parkland Hospital, the perinatal mortality rate was 32 per 1000
births in women with hypertension severe enough to require
treatment (Morgan, 2016a). As expected, the highest rates are
in women who develop superimposed preeclampsia, or whom
the risk doubles (Al Khala, 2021; Grover, 2021).
I diabetes coexists with chronic hypertension, preterm
delivery, etal-growth restriction, and perinatal mortality rates
are increased even more (Yanit, 2012). Last, children born to
women with chronic hypertension have long-term endocrine
and metabolic morbidities, specically obesity (Imterat, 2020).
Tis epigenetic eect o hypertension and o other maternal
chronic diseases is detailed in Chapter 47 (p. 831).
MANAGEMENT DURING PREGNANCY
Chronic hypertension management aims to prevent moderate
or severe hypertension, to delay or dampen superimposed preeclampsia, and to reduce rates o adverse maternal or perinatal
outcomes. Blood pressure sel-monitoring is encouraged, but or
accuracy, automated devices must be properly calibrated (Whelton, 2018). Dietary counseling and reduction o behaviors such
as tobacco, alcohol, cocaine, or other substance use serve as
early interventions. A low-sodium diet and low-dose aspirin are
others (Battarbee, 2020; Chaemsaithong, 2020). Last, pharmacologic therapy is instituted to maintain blood pressures within
suitable ranges, which are outlined later (p. 951).
Some women—especially those with long-term or untreated
hypertension—have complications that raise the risk o adverse
pregnancy events. Concentric ventricular hypertrophy and proteinuria are concerns in these women. (Ambia, 2017, 2019; Kim,
2016; Morgan, 2016a,b). Tus, early in prenatal care, cardiovascular and renal baseline unctions are assessed with echocardiogram and a 24-hour urine collection or protein measurement.
■ Antihypertensive Drugs
reatment o hypertension during pregnancy has included
every drug class, but inormation is still limited regarding saety
and efcacy (American College o Obstetricians and Gynecologists 2013, 2018a). Some commonly used drugs are listed in
Table 53-4 and the ollowing summary is abstracted rom several sources, including the 2020 Prescribers’ Digital Reerence.
Possible etal eects o many o these drugs are also discussed
in Chapter 8.
FIGURE 53-3 Frequency of selected adverse maternal and perinatal outcomes by blood pressure stratification in women with mild
chronic hypertension. SGA = small for gestational age.Chronic Hypertension 949
CHAPTER 53
Adrenergic Receptor–Blocking Agents
Peripherally acting β-adrenergic-receptor blockers cause a generalized decline in sympathetic tone and lower cardiac output.
Examples are propranolol (Inderal) and metoprolol (Lopressor,
oprol). Atenolol is not recommended because o its link with
etal-growth restriction (Bello, 2021). Labetalol (Normodyne)
is an α/β-adrenergic blocker that is considered sae. Clonidine
(Catapres) and α-methyldopa (Aldomet) act centrally by reducing sympathetic outow to eect a generalized decreased vascular tone. Drugs in this class most requently used in pregnancy
are methyldopa and labetalol (American College o Obstetricians and Gynecologists, 2018a).
Calcium Channel–Blocking Agents
Tese drugs are divided into three subclasses based on their
calcium-channel actions. Common agents include niedipine (Procardia, Adalat)—a dihydropyridine—and verapamil
(Calan)—a phenylalkyl amine derivative. Tese agents have
negative inotropic eects and thus worsen ventricular dysunction and congestive heart ailure. Teoretically, they may potentiate the vasoactive actions o magnesium sulate administered
or eclampsia neuroprophylaxis. Webster and coworkers (2017)
ound niedipine equally eective as labetalol or treatment o
chronic hypertension in pregnancy. However, those treated with
niedipine advantageously had less blood pressure variation than
those treated with labetalol (Shawkat, 2018). Although data are
limited, calcium channel–blocking agents appear to be sae therapy or chronic hypertension during pregnancy (American College o Obstetricians and Gynecologists, 2018a; Briggs, 2022).
Diuretics
Tiazide diuretics are sulonamides, and these were the rst drug
group used to successully treat chronic hypertension. Tese
agents and loop-acting diuretics such as urosemide (Lasix) are
commonly used in nonpregnant patients. Short term, they provide sodium and water diuresis with volume depletion. Over
time, there is sodium escape, and volume depletion partially
corrects. Some aspect o lowered peripheral vascular resistance
likely contributes to their eectiveness in reducing long-term
morbidity (Umans, 2015).
Tiazide drugs may be mildly diabetogenic, and the normal expected volume expansion o pregnancy may be curtailed
(Sibai, 1984). Although rates o adverse perinatal outcomes are
not greater with diuretic use, concerns have curtailed diuretic
use as rst-line therapy or chronic hypertension in pregnancy
and particularly ater 20 weeks’ gestation (Working Group
Report, 2000). Overall, thiazide diuretics are considered sae in
pregnancy (Briggs, 2022).
Vasodilators
Hydralazine (Apresoline) relaxes arterial smooth muscle and has
been used parenterally or decades to saely treat severe peripartum hypertension (Chap. 41, p. 722). However, oral hydralazine monotherapy or chronic hypertension is not generally
used because o its weak antihypertensive eects and resultant
tachycardia. It is employed as an eective vasodilator adjunct
or long-term use with other antihypertensives in women with
chronic renal insufciency or ventricular dysunction.
Angiotensin-Converting Enzyme Inhibitors
Tese drugs inhibit the conversion o angiotensin-I to the
potent vasoconstrictor angiotensin-II. Tey can cause severe
etal malormations when given in the second and third trimesters. Tese include oligohydramnios, hypocalvaria, and renal
dysunction (Chap. 8, p. 150). Some preliminary studies also
suggest teratogenic eects (Hoeltzenbein, 2018). Tey are not
recommended at any time during pregnancy (Briggs, 2022).
Angiotensin-receptor blockers act in a similar manner. However, instead o blocking the production o angiotensin-II, they
inhibit binding to its receptor. Tey are presumed to have the
same adverse etal eects as angiotensin-converting enzyme
inhibitors and also are contraindicated in pregnancy.
TABLE 53-4. Some Antihypertensive Drugs Used for Treatment of Chronic Hypertension
During Pregnancya
Drug Comment
Adrenergic-receptor agentsb
β-blockers: propranolol, metoprolol
α/β-blocker: labetalol
α-agonist: methyldopa
Avoid with asthma, decompensated heart function
Less effective for severe hypertension; sedative side effects
Calcium-channel blocking agentsb
Nifedipine, amlodipine, verapamil Avoid with tachycardia
Diureticc
Hydrochlorothiazide Begin before 20 weeks’ gestation
Vasodilating agentc
Hydralazine Hypertension complicated by cardiac or renal
dysfunction; less effective with severe hypertension
aDrugs compatible with pregnancy (Briggs, 2022).
bFirst-line agents.
cSecond-line agents.950
Section 12
Medical and Surgical Complications
■ Antihypertensive Treatment in Pregnancy
Mild or Moderate Hypertension
Initiating or continuing prepregnancy antihypertensive treatment during pregnancy is debatable or women with mild or
moderate hypertension (see able 53-1). In older observational
reports, most pregnancy outcomes were generally good in
women with untreated mild to moderate hypertension. However, these studies were relatively small and had widely varying inclusion and outcome criteria. More recently, a Cochrane
review o approximately 5000 women with mild to moderate
hypertension reported that the risk or severe hypertension in
these individuals with initially milder hypertension declined
with therapy (Abalos, 2018). Te requencies o superimposed
preeclampsia, preterm birth, small-or-gestational age newborns, and perinatal mortality, however, did not dier.
Lowering blood pressure can theoretically decrease uteroplacental perusion and lead to small-or-gestational age neonates.
von Dadelszen and coworkers (2000) ound that the decline in
mean arterial pressure associated with antihypertensive therapy
was linked to a higher requency o small-or-gestational age
newborns. Other studies both conrm and reute these ndings
(Mitchell, 2019; Morgan, 2020). In two o the larger randomized trials, the incidence o growth restriction was not higher
in women randomly assigned to treatment (Gruppo di Studio
Ipertensione in Gravidanza, 1998; Sibai, 1990). Conversely,
worsening blood pressure itsel is associated with abnormal etal
growth. Also, some suggest that the drugs have a direct etal
action (Umans, 2015). Tereore, the question regarding treatment o mild to moderate chronic hypertension in pregnancy
is yet to be resolved.
Severe Chronic Hypertension
As classied by the American College o Obstetricians and
Gynecologists (2018a), severe hypertension includes a systolic
pressure ≥160 mm Hg or a diastolic pressure ≥110 mm Hg.
reatment should be initiated or persistent severe hypertension to reduce maternal morbidity and mortality risks (Akbar,
2019). In women with cardiovascular or renal end-organ damage, treatment may be instituted at systolic pressures ≥140 to
150 mm Hg or diastolic pressures ≥90 to 100 mm Hg in an
attempt to mitigate urther damage.
Women whose hypertension is severe enough to require
antihypertensive therapy or cause end-organ damage carry
an increased risk or superimposed preeclampsia. In an older
study, Sibai and coworkers (1986) described outcomes rom 44
pregnancies in women whose blood pressure at 6 to 11 weeks’
gestation was ≥170/110 mm Hg. All were given oral treatment
with α-methyldopa and hydralazine to maintain pressures
<160/110 mm Hg. Hal o these women developed superimposed preeclampsia, and all adverse perinatal outcomes were
in this group. Conversely, those women with severe chronic
hypertension who did not develop superimposed preeclampsia
had reasonably good outcomes. Morgan and colleagues (2016a)
conrmed these ndings in their study o 447 women requiring
treatment or chronic hypertension prior to 20 weeks.
Cardiac abnormalities and renal insufciency resulting rom
uncontrolled hypertension raise the risk or adverse pregnancy
outcomes. Women with baseline proteinuria >300 mg/d have
higher rates o superimposed preeclampsia, preterm birth, and
small-or-gestational age neonates compared with those whose
24-hour protein excretion is <300 mg/d (Table 53-5) (Morgan, 2016b). Abnormal cardiac remodeling and let ventricular
hypertrophy also are associated with superimposed preeclampsia, preterm birth, and neonatal ICU admission (Ambia, 2018,
2019).
“Tight Control”
During the past decade, the concept o tight control o blood
pressure has been advocated to optimize maternal and perinatal outcomes. Such control is analogous to that o glycemic
control or diabetes management. Te observational study by
TABLE 53-5. Selected Pregnancy Outcomes in Women with Chronic
Hypertension with and without Baseline Proteinuriaa and
Who Were Treated During Pregnancy
Outcome
Baseline
Proteinuriaa No Proteinuria p value
Superimposed preeclampsia 79% 49% <0.001
Abruption 0 1% 0.45
EGA at delivery (mean)b 35.1 ± 4.3 wk 37.2 ± 3.3 wk <0.001
≤30 weeks
≤34 weeks
≤37 weeks
18%
34%
48%
6%
17%
26%
0.001
0.005
0.002
Birthweight (mean)b
≤3rd percentile
≤10th percentile
2379 ± 1028 g
20%
41%
2814 ± 807 g
9%
22%
<0.001
0.01
<0.001
Perinatal mortality 36/1000 31/1000 0.47
aDefined as ≥300 mg/d protein excretion before 20 weeks’ gestation.
bMean ± standard deviations.
EGA = estimated gestational age.Chronic Hypertension 951
CHAPTER 53
Ankumah and colleagues (2014) noted earlier lends credence
to tighter blood pressure control. Tey showed that the adverse
pregnancy outcome risk was lower when blood pressures beore
20 weeks’ gestation were <140 mm Hg compared with higherpressure categories and increasing blood pressures.
Unortunately, those observations were not conrmed.
Magee and associates (2015) randomized 987 women to
either less-tight or tight control o hypertension. Except or
a lower rate o severe hypertension in the tightly controlled
group, other outcomes between these two groups did not dier
(Table 53-6). Analyzing the same cohort, no gestational age
was identied at which tight control was preerable (Pels,
2018). A systematic review reported similar results (Panaitesc,
2017). At this time, no proven benets or risks are attributed
to “tight”—target diastolic pressure <85 mm Hg—versus
“less-tight”—target diastolic pressure <100 mm Hg—control
o chronic hypertension during pregnancy (American College
o Obstetricians and Gynecologists (2018a). A randomized
trial—Project CHAP—is ongoing to help address this question
(U.S. National Library o Medicine, 2020).
Recommendations for Therapy
Until the treatment o uncomplicated mild to moderate chronic
hypertension in pregnancy is conrmed to have benets, it
seems reasonable to ollow the guidelines o the American College o Obstetricians and Gynecologists (2018a) and the Society
or Maternal-Fetal Medicine (2015). Tus, pregnant women
with severe hypertension must be treated or maternal neuro-,
cardio-, and renoprotection. reatment is also mandatory or
women with prior adverse outcomes such as a stroke, myocardial inarction, and evidence or cardiac or renal dysunction.
Many nd it reasonable to begin antihypertensive treatment in otherwise healthy pregnant women with persistent
systolic pressures >150 mm Hg or diastolic pressures >95 to
100 mm Hg (August, 2015; Webster, 2017). Drugs commonly
used are listed in able 53-4. At Parkland Hospital, we initiate treatment with antihypertensive agents at blood pressures
≥150/100 mm Hg. Our preerred regimens include monotherapy with a β-blocking drug such as labetalol or a calcium
channel–blocking agent such as niedipine or amlodipine (Norvasc). Adjunct therapy with a thiazide diuretic seems reasonable
or women in the rst hal o pregnancy. Tis is more bene-
cial in black women, in whom the prevalence o salt-sensitive
chronic hypertension is high.
Controversy surrounds women who present early in pregnancy and who are already taking antihypertensive drugs (Rezk,
2016). According to the American College o Obstetricians
and Gynecologists (2018a) and the Society or Maternal-Fetal
Medicine (2015), or women with mild to moderate hypertension, it is reasonable to discontinue medications during the rst
trimester and to restart them i blood pressures approach the
severe range. At Parkland Hospital, we continue treatment i
the woman is already taking medications when she presents or
prenatal care. As exceptions, angiotensin-converting enzyme
inhibitors and angiotensin-receptor blockers are stopped.
Some women will have persistently worrisome hypertension despite usual therapy. In these women, development o
superimposed preeclampsia becomes a primary concern and is
detailed next. Other possibilities include inaccurate blood pressure measurements, suboptimal treatment, illicit drug use, and
antagonizing substances such as chronic ingestion o nonsteroidal
antiinammatory drugs (NSAIDs) (Moser, 2006; Sowers, 2005).
■ Superimposed Preeclampsia
As discussed in Chapter 40 (p. 690), conditions that support
the diagnosis o superimposed preeclampsia include worsening
hypertension, new-onset proteinuria, neurological symptoms
such as severe headaches and visual disturbances, generalized
edema, oliguria, and certainly, convulsions or pulmonary edema.
Tese same criteria apply to women with chronic hypertension.
However, preeclampsia can be difcult to diagnose in a
chronically hypertensive woman. First, blood pressures may
increase during pregnancy in women with chronic hypertension
alone and without superimposed preeclampsia. Tis is most
commonly encountered near the end o the second trimester.
In the absence o other supporting criteria or superimposed
preeclampsia, this likely represents the higher end o the normal
blood-pressure curve shown in Figure 53-1. In such women, i
preeclampsia is excluded, it is reasonable to begin or to increase
the dose o antihypertensive therapy.
As a second diagnostic obstacle, many chronically hypertensive patients have preexisting end-organ damage and laboratory
values that mimic preeclampsia. New-onset proteinuria is consistent with the diagnosis o superimposed preeclampsia. However, this is not applicable to women who have underlying renal
disease with chronic proteinuria (Cunningham, 1990; Morgan,
2016b). In these women, diagnosing superimposed preeclampsia based on worsening proteinuria is problematic. Laboratory
abnormalities that support preeclampsia include rising serum
creatinine or hepatic transaminase levels, thrombocytopenia, or
any o the acets o HELLP (hemolysis, elevated liver enzyme
levels, low platelet count) syndrome. For women with chronic
TABLE 53-6. Selected Maternal and Perinatal Outcomes
in Pregnant Women with Chronic
Hypertension According to Less-Tight
versus Tight Control
Outcome
Less-Tight
Control Tight Control
Maternal
Placental abruption
Severe hypertensiona
Preeclampsia
HELLP syndrome
2.2%
41%
49%
1.8%
2.3%
28%
46%
0.4%
Perinatal
Deaths
Weight <10th percentile
Weight <3rd percentile
Respiratory problem
28/1000
16%
4.7%
17%
23/1000
20%
5.3%
14%
a
p <0.001, all other comparisons p >0.05.
HELLP = hemolysis, elevated liver enzyme levels, low
platelet count.952
Section 12
Medical and Surgical Complications
hypertension and superimposed preeclampsia with severe eatures, magnesium sulate or maternal neuroprophylaxis is recommended (Chap. 41, p. 719).
Expectant Management of Early-Onset Preeclampsia
Given that 40 to 50 percent o cases o superimposed preeclampsia develop early and beore 37 weeks, considerations or expectant management to allow etal maturation may be reasonable
(Harper, 2016). However, most maternal outcomes are better
when women with superimposed preeclampsia are delivered,
even when the etus is markedly preterm. Increased risk or placental abruption, cerebral hemorrhage, and peripartum heart ailure attend delivery delays (Cunningham, 1986, 2005; Martin,
2005). And prolonged expectant management is associated with
an increased risk o maternal cardiac disease in the ensuing years
(Rosenbloom, 2020). In a study rom Magee-Women’s Hospital,
42 o 68 careully selected women with a median gestational age
o 31.6 weeks were expectantly managed (Samuel, 2011). Despite
liberal criteria to mandate delivery, 17 percent o these mothers
developed either placental abruption or pulmonary edema. Te
latency period was extended by a mean o 10 days. Tere were no
perinatal deaths, however, neonatal outcomes were no better than
those in the group delivered immediately. Women with superimposed preeclampsia beore 34 weeks’ gestation may be candidates
or expectant management at acilities with adequate maternal
and neonatal ICU resources (American College o Obstetricians
and Gynecologists, 2018a). At Parkland Hospital, we pursue
delivery when superimposed preeclampsia is diagnosed.
■ Fetal Assessment
Because o greater stillbirth and etal-growth restriction risks,
antepartum etal surveillance is recommended or women with
chronic hypertension. However, data are limited regarding
which subpopulations with chronic hypertension benet most.
Te ideal test, testing interval, and gestational age o initiation
are other unknowns (American College o Obstetricians and
Gynecologists, 2018a; Freeman, 2008).
All women with chronic hypertension should undergo a
sonographic etal-growth assessment in the third trimester.
Additionally, Chahine and colleagues (2019) recommend that
women with low-risk disease undergo weekly antepartum testing. Tey dened low-risk by our criteria: (1) women ≤35
years o age, (2) mild- to moderate-range blood pressures not
requiring medication, (3) no prior hypertension-related adverse
pregnancy outcomes, and (4) no end-organ damage. For antepartum testing, a nonstress test or a biophysical prole is suitable (Chap. 20, p. 392).
Women with high-risk disease ail to meet these our criteria. For them, sonography and antepartum testing are considered earlier, and the value o these tools to assess etal-growth
restriction is detailed in Chapter 47 (p. 830). One surveillance
algorithm or suspected etal-growth restriction is outlined in
Figure 47-6 (p. 829).
■ Delivery Timing
For women with mild to moderate chronic hypertension who
have an otherwise uncomplicated pregnancy, the American
College o Obstetricians and Gynecologists (2018a) recommends waiting or delivery until 37 to 38 weeks’ gestation.
Women taking antihypertensive drugs are not delivered beore
370/7 weeks, and those not receiving drug treatment are delivered no earlier than 380/7 weeks. A nationally convened consensus committee recommended consideration or delivery at 38
to 39 weeks, that is, ≥37 completed weeks (Spong, 2011). A
large population-based Canadian study showed similar results
(Ram, 2018). Expectant management beyond 39 weeks’ gestation is associated with an increasing incidence o severe preeclampsia, and planned delivery beore 37 weeks was associated
with a rise in rates o adverse neonatal outcomes (Harper, 206).
For women who have etal-growth restriction, the decision
to deliver incorporates clinical judgment. Maternal health is
balanced against estimated etal weight, gestational age, and
chance o neonatal survival.
■ Intrapartum Considerations
For women with chronic hypertension, obstetrical actors dictate delivery route. Magnesium sulate is not given unless there
is superimposed severe preeclampsia. Epidural analgesia is ideal
but does not substantively lower blood pressure. A trial o labor
induction is preerable, and many o these women will deliver
vaginally (Alexander, 1999; Atkinson, 1995). Similarly, or the
growth-restricted etus, delivery route is based on obstetrical
actors. However, many etuses with growth restriction exhibit
nonreassuring etal heart rate patterns and require cesarean
delivery (McKinney, 2016).
For women with superimposed preeclampsia, intrapartum
management mirrors that described in Chapter 41 (p. 719).
Tese women may have a longer rst-stage labor (BregandWhite, 2017). Epidural analgesia or labor and delivery is
optimal, but it is not provided with the intent to treat hypertension (Lucas, 2001). Tat said, women with superimposed
preeclampsia are more sensitive to the acute hypotensive eects
o epidural analgesia (Vricella, 2012). Magnesium sulate neuroprophylaxis is initiated or eclampsia prevention. Severe
hypertension—diastolic blood pressure ≥110 mm Hg or
systolic pressure ≥160 mm Hg—is treated with either intravenous hydralazine, intravenous labetalol, or oral niedipine.
Some preer to treat women when the diastolic pressure reaches
100 to 105 mm Hg. Vigil-De Gracia and coworkers (2006)
randomly assigned 200 gravidas to receive intravenous hydralazine or labetalol to acutely lower severe high blood pressure.
Outcomes were similar except or signicantly higher rates o
maternal palpitations and tachycardia with hydralazine and signicantly greater rates o neonatal hypotension and bradycardia
with labetalol.
■ Postpartum Care
Prevention and management o adverse postpartum complications is similar in women with severe chronic hypertension
and in those with severe preeclampsia–eclampsia. For persistent severe hypertension, consideration is given to causes such
as pheochromocytoma or Cushing disease (Sibai, 2012). In
women with chronic end-organ damage, certain complicationsChronic Hypertension 953
CHAPTER 53
are more common. Tese include cerebral or pulmonary edema,
heart ailure, renal dysunction, or cerebral hemorrhage, especially within the rst 48 hours ater delivery. Tese requently
are preceded by sudden elevations o mean arterial blood pressure, especially o the systolic component (Cunningham, 2000,
2005; Martin, 2005).
Following delivery, as maternal peripheral resistance rises,
let ventricular workload also grows. Tis elevation is urther
aggravated by appreciable and pathological amounts o interstitial uid that are mobilized to be excreted as endothelial disruption rom preeclampsia resolves. In these women, sudden
hypertension—either moderate or severe—may exacerbate diastolic dysunction, cause systolic dysunction, and lead to pulmonary edema (Cunningham, 1986; Gandhi, 2001). Prompt
hypertension control, along with urosemide-evoked diuresis,
usually quickly resolves pulmonary edema.
Te antihypertensive regimen given antepartum may be
continued in the puerperium. In untreated women, labetalol or niedipine can also be used or persistent hypertension (Sharma, 2017). It also is possible in many women to
orestall postpartum hypertension by administering intravenous or oral urosemide to augment normal postpartum
diuresis. In one study, 20 mg oral urosemide given daily or
5 days to postpartum women with severe preeclampsia aided
blood pressure control (Ascarelli, 2005). A recent randomized trial showed that daily urosemide decreased the need
or antihypertensive therapy at hospital discharge (Perdigao,
2020). Daily weights are helpul in this regard. On average,
a woman should weigh 15 pounds less immediately ater
delivery. Excessive extracellular uid can then be estimated
by comparing her last prenatal weight plus 15 pounds against
the puerpera’s current weight.
Some evidence supports that chronic ingestion o NSAIDs
in the puerperium elevates blood pressure in women with
severe preeclampsia (Vigil-De Gracia, 2017). Tis may not be
problematic i these drugs are given only intermittently and
as needed (Blue, 2018). Postpartum admission rates or severe
hypertension approximate 1.5 percent (Chornock, 2021).
Discussion o postpartum contraception may begin prior to
delivery. As described in Chapter 38 (p. 672), certain methods
are less ideal or contraindicated or some women with chronic
hypertension. Moreover, or puerpera at highest risk or uture
pregnancy complications, the Society or Maternal–Fetal Medicine (2019) encourages immediate postpartum long-acting
reversible contraceptive (LARC) insertion or suitable candidates.
■ LongTerm Prognosis
Women with chronic hypertension are at high risk or lietime
cardiovascular complications, especially when accompanied
by diabetes, obesity, and the metabolic syndrome. Persistent
hypertension 3 years ater severe preeclampsia was associated
with a thicker let-ventricular septum compared with women
who became normotensive (Vaught, 2019). Te lietime cardiovascular morbidity and mortality risks associated with
hypertensive disorders o pregnancy are discussed in Chapter
41 (p. 726) (Wu, 2021).
R
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