HYPERTENSION IN PREGNANCY

1. Background
Hypertension is the most common medical problem encountered during
pregnancy, complicating 2-3% of pregnancies. Hypertensive disorders during
pregnancy are classified into 4 categories, as recommended by the National High
Blood Pressure Education Program Working Group on High Blood Pressure in
Pregnancy:
1) Chronic hypertension,
Hypertension that predates pregnancy
2) Preeclampsia-eclampsia
Hypertension and proteinuria. in the absence of proteinuria, preeclampsia
is diagnosed as hypertension in association with thrombocytopenia (AT
<100.000/L), impaired liver function 9elevated blood level of liver
transaminases to twice the normal concentration), the new development of
renal insufficiency (elevated serum creatitnine greater than 1.1 mg/dL or a
doubling of serum creatinine in the absence of renal disease), pulmonary
edema, or new-onset cerebral or visual disturbance
3) Preeclampsia superimposed on chronic hypertension
Chronic hypertension in association with preeclampsia
4) Gestational hypertension
Transient hypertension of pregnancy or chronic hypertension identified in
the latter half of pregnancy.1

This terminology is preferred over the older but widely used term pregnancy-
induced hypertension (PIH) because it is more precise.

The Society of Obstetricians and Gynecologists of Canada (SOGC) recently

released revised guidelines that simplified the classification of hypertension in
pregnancy into 2 categories, preexisting or gestational, with the option to add
"with preeclampsia" to either category if additional maternal or fetal symptoms,
signs, or test results support this.2

Chronic hypertension is defined as blood pressure exceeding 140/90 mm Hg

before pregnancy or before 20 weeks' gestation. When hypertension is first
identified during a woman's pregnancy and she is at less than 20 weeks' gestation,
blood pressure elevations usually represent chronic hypertension. In contrast, new
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 onset of elevated blood pressure readings after 20 weeks' gestation mandates the
consideration and exclusion of preeclampsia. Preeclampsia occurs in up to 5% of
all pregnancies, in 10% of first pregnancies, and in 20-25% of women with a
history of chronic hypertension. Hypertensive disorders in pregnancy may cause
maternal and fetal morbidity, and they remain a leading source of maternal
mortality.

2. Epidemiology
In United States, Chronic hypertension occurs in up to 22% of women of
childbearing age, with the prevalence varying according to age, race, and body
mass index. Population-based data indicate that approximately 1% of pregnancies
are complicated by chronic hypertension, 5-6% by gestational hypertension
(without proteinuria), and 1-2% by preeclampsia.

Black women have higher rates of preeclampsia complicating their pregnancies

compared with other racial groups, mainly because they have a greater prevalence
of underlying chronic hypertension. Among women aged 30-39 years, chronic
hypertension is present in 22.3% of African Americans, 4.6% of non-Hispanic
white persons, and 6.2% of Mexican Americans. Hispanic women generally have
blood pressure levels that are the same as or lower than those of non-Hispanic
white women.

3. Pathophysiology
3.1. Chronic Hypertension
Chronic hypertension may be either essential (90%) or secondary to some
identifiable underlying disorder, such as renal parenchymal disease (eg,
polycystic kidneys, glomerular or interstitial disease), renal vascular disease
(eg, renal artery stenosis, fibromuscular dysplasia), endocrine disorders (eg,
adrenocorticosteroid or mineralocorticoid excess, pheochromocytoma,
hyperthyroidism or hypothyroidism, growth hormone excess,
hyperparathyroidism), coarctation of the aorta, or oral contraceptive use.

About 20-25% of women with chronic hypertension develop preeclampsia

during pregnancy.

3.2. Pre-eclampsia

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 Although the exact pathophysiologic mechanism is not clearly understood,
preeclampsia is primarily a disorder of placental dysfunction leading to a
syndrome of endothelial dysfunction with associated vasospasm. In most
cases, pathology demonstrates evidence of placental insufficiency with
associated abnormalities such as diffuse placental thrombosis, an
inflammatory placental decidual vasculopathy, and/or abnormal
trophoblastic invasion of the endometrium. This supports abnormal
placental development or placental damage from diffuse microthrombosis as
being central to the development of this disorder.

The widespread endothelial dysfunction may manifest as a maternal

syndrome, fetal syndrome, or both. Endothelial damage leads to pathologic
capillary leak that can present in the mother as rapid weight gain,
nondependent edema (face or hands), pulmonary edema,
hemoconcentration, or a combination thereof. The diseased placenta can
also affect the fetus via decreased utero-placental blood flow. This decrease
in perfusion can manifest clinically as nonreassuring fetal heart rate testing,
low scores on a biophysical profile, oligohydramnios, or as fetal growth
restriction.
The hypertension occurring in preeclampsia is due primarily to vasospasm,
with arterial constriction and relatively reduced intravascular volume
compared to normal pregnancy. The vasculature of normal pregnant women
typically demonstrates decreased responsiveness to vasoactive peptides such
as angiotensin-II and epinephrine. In contrast, women who develop
preeclampsia typically show a hyperresponsiveness to these hormones, an
alteration that may be seen even before the hypertension and other
manifestations of preeclampsia become apparent. In addition, blood
pressures in preeclampsia are labile, and the normal circadian blood
pressure rhythms may be blunted or reversed. One study found increased
arterial stiffness in women with preeclampsia, as well as in those with
gestational hypertension, compared with normotensive controls; treatment
with alpha methyldopa significantly improved the vascular stiffness in
preeclampsia but did not normalize it.3
3.3. Gestational Hypertension

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 Gestational hypertension refers to hypertension with onset in the latter part
of pregnancy (>20 weeks gestation) without any other features of
preeclampsia, and followed by normalization of the blood pressure
postpartum. Of women who initially present with apparent gestational
hypertension, about one third develop the syndrome of preeclampsia. As
such, these patients should be observed carefully for this progression. The
pathophysiology of gestational hypertension is unknown, but in the absence
of features of preeclampsia, the maternal and fetal outcomes are usually
normal. Gestational hypertension may, however, be a harbinger of chronic
hypertension later in life.

REFERENCES
1. Report of the National High Blood Pressure Education Program Working Group on
High Blood Pressure in Pregnancy. Am J Obstet Gynecol. Jul 2000;183(1):S1-S22.

2. Magee LA, Helewa M, Moutquin J-M et al. Diagnosis, Evaluation, and Management
of the Hypertensive Disorders of Pregnancy. Journal of Obstetrics and Gynaecology
Canada [serial online]. March 2008;30:S1-S48. Accessed July 10, 2009. Available at
http://www.sogc.org/guidelines/documents/gui206CPG0803_001.pdf.

3. Khalil A, Jauniaux E, Harrington K. Antihypertensive therapy and central

hemodynamics in women with hypertensive disorders in pregnancy. Obstet
Gynecol. Mar 2009;113(3):646-54.

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4. Poon LC, Kametas NA, Maiz N, Akolekar R, Nicolaides KH. First-trimester
prediction of hypertensive disorders in
pregnancy. Hypertension. May 2009;53(5):812-8.

5. American Association of Clinical Endocrinologists medical guidelines for clinical

practice for the diagnosis and treatment of hypertension. National Guideline
Clearinghouse. Available at http://www.guideline.gov/summary/summary.aspx?
doc_id=9338&nbr=005007. Accessed June 1, 2009.

6. Cooper WO, Hernandez-Diaz S, Arbogast PG, Dudley JA, Dyer S, Gideon PS, et
al. Major congenital malformations after first-trimester exposure to ACE inhibitors. N
Engl J Med. Jun 8 2006;354(23):2443-51.
7. Craici I, Wagner S, Garovic VD. Preeclampsia and future cardiovascular risk: formal
risk factor or failed stress test?. Ther Adv Cardiovasc Dis. Aug 2008;2(4):249-59.