DOI: 10.1097/JPN.
0b013e318223ad14
J. Perinat Neonat Nurs r Volume 25 Number 3, 245–252 r Copyright 
Preeclampsia
Pathophysiology and Implications for Care
Nancy S. Townsend, RN, MSN; Susan B. Drummond, RN, MSN
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ABSTRACT
Nurses are increasingly encountering pregnant/postpartum
women with hypertensive disorders of pregnancy, of
which preeclampsia is one of the most common. The Joint
Commission published a Sentinel Event Alert in 2010 on
prevention of maternal death. This report notes that one
of the 5 leading causes of pregnancy-related mortality
between 1991 and 1997 was “hypertensive disorder.”
Preeclampsia presents significant risk to the health of the
mother and the fetus. Clearly, nurses must understand the
pathophysiology, assessment, management, recurrence
risk, and long-term implications of preeclampsia to
participate fully in a management plan that promotes safe
patient care.
Key Words: hypertension, magnesium sulphate,
preeclampsia
ypertension in pregnancy is a serious com-
H
plication, which may lead to significant mor-
bidity and even death for the mother and fe-
tus. Nurses are increasingly encountering pregnant/
postpartum women with hypertensive disorders of
pregnancy.1,2 This trend, combined with the potential
sequelae of preeclampsia, render astute nursing assess-
ment, and intervention critical in caring for childbear-
ing families. Nurses need to consider current research
Author Affiliations: The Junior League Fetal Center at Vanderbilt,
(Ms. Townsend); and Department of Obstetrics and Gynecology,
Vanderbilt University Medical Center, Nashville, TN (Ms. Drummond).
Disclosure: The authors have disclosed that they have no significant
relationships with, or financial interest in, any commercial companies
pertaining to this article.
Corresponding Author: Nancy S. Townsend, RN MSN, The Junior
League Fetal Center at Vanderbilt, Monroe Carell Jr. Children’s Hospital,
2200 Children’s Way, Doctor’s Office Tower, 6th Floor, Nashville, TN
37232 (nancy.s.townsend@vanderbilt.edu).
Submitted for publication: March 1, 2011 Accepted for publication:
May 10, 2011
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C 2011 Wolters Kluwer Health | Lippincott Williams & Wilkins
on pathophysiologic principles and treatment options
to advocate for evidence-based care. This knowledge
will also provide a framework from which nurses may
counsel their patients.3 Furthermore, mastery of current
evidence gives nurses an opportunity to intervene by
providing strategies for risk factor modification in the
prevention of cardiovascular disease.4 Although a full
discussion of all suspected pathyphysiologic mecha-
nisms, assessment, and treatment options involved in
all hypertensive disorders in pregnancy is beyond the
scope of this article, an update on pathophysiology,
possible modes of prevention, assessment, manage-
ment, and long-term implications of preeclampsia will
be presented.
UPDATE ON PATHOPHYSIOLOGY
Although the cause(s) of preeclampsia remains un-
known, much research effort has been exerted on study
of the pathophysiologic mechanisms.5 – 9 What is known
is that the placenta or the maternal adaptation to pla-
cental invasion and remodeling of uterine arteries is a
factor in the development of preeclampsia. Therefore,
this condition begins at conception, not at the onset
of visible symptoms. The placentation in preeclamp-
sia appears to be incomplete in preeclamptic women.
At the beginning of a normal pregnancy, the placenta
should cause remodeling of the uterine spiral arteries,
which then allows for the necessary increased blood
and oxygen flow required in pregnancy. This is accom-
plished as the cytotrophoblast cells invade the endothe-
lium and musculature of the maternal spiral arteries
resulting in large capacity vessels with low resistance.
Research has shown that pregnancies complicated by
preeclampsia are notable for an incomplete transforma-
tion of these spiral arteries as the cytotrophoblast cells
infiltrate the decidual portion of the spiral arteries but
fail to penetrate the myometrial portion resulting in nar-
row vessels and hypoperfusion.7,10 This together with
placental infarction can ultimately lead to decreased
www.jpnnjournal.com 245
oxygen delivery to the placenta and thus placental
hypoxia.11
Once this poor placentation process begins, the
pregnancy usually is affected by the common maternal
complications, depending on (1) the extent of the in-
flammatory process and (2) the maternal response to
those inflammatory signals.10 The systemic maternal dis-
ease process is associated with endothelial cell dys-
function caused by a “hyperinflammatory” state lead-
ing to production of substances known as inflamma-
tory cytokines. The resulting endothelial dysfunction is
associated with higher vascular reactivity; all of which
preceed the onset of the typical maternal symptoms.5
Considering that blood vessel walls are lined with en-
dothelium, and endothelial dysfunction is a hallmark
of preeclampsia, the damage in this endothelial lining
leads to a decrease in colloid oncotic pressure through
leakage of protein molecules from the intravascular
compartment to the extravascular space.
Loss of optimal endothelial function is also associ-
ated with the hemostatic changes seen in preeclampsia.
Elevated fibronectin levels, which are evidence of en-
dothelial damage, have been documented in women
with preeclampsia. In some studies, these high fi-
bronectin levels were evident prior to the develop-
ment of symptomatic preeclampsia.6,12 More recently,
it has been shown that circulating levels of the protein
known as soluble endoglin has been found to be asso-
ciated with preeclampsia. Circulating levels of soluble
endoglin increase significantly before the onset of clin-
ically diagnosed preeclampsia.13 Although it has been
known for years that preeclampsia may be present long
before the clinical signs and symptoms appear, ongo-
ing, and emerging research continues to support this
hypothesis.
It is well established that preeclampsia is associated
with vasospasm, abnormal hemostasis, and activation of
the coagulation system. Platelet activation and platelet
consumption in the microvasculature play key roles
in the hemostasis/coagulation process.7 When platelets
come into contact with damaged endothelium, the clot-
ting cascade is initiated and platelets are activated, re-
sulting in clot formation. The endothelial dysfunction
classic in preeclampsia pathology is also responsible for
vasoconstriction because of the imbalance in thrombox-
ane and prostacyclin with thromboxane being respon-
sible for the vasoconstriction.
It has been proposed that preeclamptic pregnancies
exhibit a “hyperdynamic flow” state in early pregnancy.
That is, pregnancies destined to develop preeclampsia
exhibit an exaggerated hemodynamic response to the
normal vascular changes in pregnancy (ie, increased
blood flow/low vascular resistance). Some women des-
tined to develop preeclampsia exhibit an exaggeration
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of this high flow/low resistance state long before clini-
cal symptoms of preeclampsia appear.8,14 It is thought
that the endothelial damage seen in preeclampsia may
be caused by the exposure of capillary beds to these
exaggerated low vascular pressures and high cardiac
output in early pregnancy.15
Sibai et al,10 point out that the inflammatory sig-
nal processing seen in preeclampsia may depend on
fetal genes whereas the maternal response to the in-
flammatory signals would depend on maternal genes.
The connection to genetics is further supported by the
fact that male children of preeclamptic pregnancies are
twice as likely to go on to be a father of a preeclamptic
pregnancy.16 Also, a woman who becomes pregnant by
a man whose previous partner had preeclampsia is at a
higher risk of developing the syndrome than if the pre-
vious partner was normotensive during pregnancy. This
implies that both maternal and fetal genes are involved
in this unique disease process.10,16 – 18
Research aimed at understanding the maternal and
paternal genetic influences on the development of
preeclampsia is likely to continue.
One newer method of investigating pathophysiology
is to study the patterns of gene expression in normal
tissues as compared to tissues from individuals affected
by this disease (ie, comparing blood or placental tis-
sue of normal pregnant women to that of preeclamptic
women).
Currently, the exact genes involved in preeclampsia
are not known. One way to investigate this is through a
technology called microarray. Microarray is a tool used
to study many genes or gene products in an experi-
ment. This state-of-the-art technology is currently being
used in obstetric practice as well as other clinical set-
tings, though it is too early to apply to preeclamptic
women specifically. The hope is that microarray tech-
nology may 1 day highlight which genes are likely
to be implicated in the development of preeclampsia.
Long term, this technology will possibly identify genes,
which may be targets for drug therapy or other treat-
ments, and allow for genetic risk assessment through
blood or buccal cell sampling. Treatments, individu-
alized for each patient, may eventually be an option
once the genes and environmental factors are better
understood.19
PREVENTION
Attempts at prevention of preeclampsia have been fo-
cused on women at higher risk for developing the
disease. These initiatives have been limited by the in-
ability to completely understand the pathophysiologic
principles. Thus, attempts at prevention have been fo-
cused on trying to correct theoretical abnormalities in
preeclampsia.7,11
July/September 2011
 Nurses can play a critical role in identifying and mon-
itoring women at high risk for preeclampsia. Multiple
modes of prevention have been investigated, includ-
ing use of low-dose aspirin, calcium supplementation,
antioxidants, and fish oil.10,20 – 23 Although there are a
multitude of studies on prevention, with some find-
ings considered controversial, there are no clear general
recommendations for the prevention of preeclampsia.
Lindheimer and Sibai20 recently suggested that research
resources for human subject study should focus on pre-
diction markers and further definition of the mecha-
nisms of preeclampsia. These authors also suggest that,
if the cause of preeclampsia is multifactorial, “the effect
of a single intervention would be diluted” and that the
development of a “preventative cocktail” for all causes
of the disease should be a precursor to the development
of future studies.
Low-dose aspirin
Aspirin is postulated to prevent preeclampsia by cor-
recting an imbalance in the ratio of thromboxane A2
(vasoconstrictor and platelet aggregator) to prostacy-
clin (vasodilator and inhibitor of platelet aggregation).
Aspirin inhibits the production of thromboxane more
than it inhibits the production of prostacyclin, thus as-
pirin has been evaluated in multiple studies to possibly
protect against the vasoconstrictive effects of throm-
boxane. A large double-blind, randomized, placebo-
controlled trial conducted in the United States en-
rolled 2539 women and found that low-dose aspirin did
not significantly reduce the incidence of preeclampsia.
Furthermore, perinatal outcomes in high-risk women
were not significantly improved.21 A review of several
large trials found that, not only did aspirin fail to im-
prove outcomes, but also did not reduce the incidence
of preeclampsia.11 Currently the American Congress of
Obstetricians and Gynecologists (ACOG) does not rec-
ommend use of low-dose aspirin in low-risk women.9
In the group of women at moderate to high risk for
developing preeclampsia, it is possible that aspirin may
be of some benefit. However, the exact group for which
low-dose aspirin therapy may be beneficial has not
been identified. It has been suggested that low-dose as-
pirin be offered on a case-to-case basis in women with
a history of preeclampsia in their previous pregnancy.24
The option of not utilizing low-dose aspirin therapy in
moderate- to high-risk women is also reasonable.25
Calcium supplementation
Rationale for the use of calcium supplementation
in preeclampsia prevention surrounded the fact that
hypocalciuria (reduced excretion of calcium in the
urine) has been associated with preeclampsia.3 Two
large randomized-controlled trials, one in the United
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States and one in Australia, evaluated the use of calcium
supplementation as a method of preventing preeclamp-
sia. Neither study showed evidence of benefit.26,27
Whereas Dekker & Sibai22 suggested that calcium sup-
plementation may be beneficial in populations with
low calcium intake, calcium supplementation is gen-
erally not currently recommended for preeclampsia
prevention.
Antioxidant supplementation (vitamin C and E,
and fish oil)
Antioxidant supplementation has been investigated
with the idea that oxidative stress may cause the en-
dothelial dysfunction seen in preeclampsia. It is known
that the levels of “buffering antioxidants” are decreased
in women destined to develop preeclampsia.28 None
of the large randomized-controlled trials evaluating vi-
tamin C and E supplementation in either high-risk or
low-risk women have shown any benefit.23,28 –,31 In
fact, concomitant supplementation with vitamins C and
E may also be associated with “an increase in ad-
verse events.”20 Thus, vitamin C and E supplementation
for prevention of preeclampsia is not currently recom-
mended.
Fish oil supplementation has been proposed as a
possible mode of preeclampsia prevention because
of its possible protective effects on blood vessels.
Although some studies actually revealed a lowering
of blood pressure (BP) and decreased incidence of
preeclampsia,32,33 the majority of evidence on fish oil
does not support its routine use for preeclampsia pre-
vention or for preventing progression of the disease
once it is diagnosed.25
ASSESSMENT
Established criteria for the diagnosis of preeclampsia
and/or severe preeclampsia are outlined in Tables 1
and 2.9
The Joint Commission, formerly known as the Joint
Commission on Accreditation of Healthcare Organiza-
tions (JCAHO), published a Sentinel Event Alert in 2010
on prevention of maternal death. This report notes that
there has been no recent decrease in overall mater-
nal mortality in the United States. In fact, 1 of the 5
Table 1. Criteria for diagnosis of
preeclampsia
BP: ≥ 140 mm Hg systolic or 90 diastolic that occurs
after 20 weeks of gestation in a woman with
previously normal BP
Proteinuria: urinary excretion of 0.3 g of protein or
higher in a 24-hour urine specimen
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Table 2. Criteria for diagnosis of severe
preeclampsia
BP: ≥ 160 mm Hg systolic or 110 diastolic on 2
occasions at least 6 hours apart while the patient is
on bed rest.
Proteinuria: ≥ 5 g in a 24-hour specimen or ≥ 3 + on 2
random urine samples collected at least 4 hours apart.
Oliguria: < 500 mL in 24 hour
Cerebral or visual disturbances
Pulmonary edema or cyanosis
Epigastric or right upper-quadrant pain
Impaired liver function
Thrombocytopenia
Fetal growth restriction
leading causes of pregnancy-related mortality between
1991 and 1997 was “hypertensive disorder.” The Joint
Commission highlighted a 2008 study, which evaluated
individual causes of maternal deaths among 1.5 million
deliveries.34 According to the study authors the most
common preventable error in caring for preeclamptic
patients was “inattention to BP control and signs or
symptoms of pulmonary edema.” Clearly, astute nurs-
ing assessment and prompt intervention by the entire
obstetric team are warranted when caring for women
with preeclampsia.
Nurses are usually the first point of assessment in a
typical obstetric practice, either in person during an of-
fice or hospital visit, or during telephone triage. Thus,
it is essential that the nursing process include a thor-
ough knowledge of the latest evidence and recommen-
dations on preeclampsia diagnosis. Nursing assessment
typically begins with a detailed history. Patients may
be queried regarding symptoms of preeclampsia, and
asked about a possible history of chronic hypertension,
renal disease, or previous preeclampsia.35
Initial assessment as an inpatient is usually rec-
ommended for all newly diagnosed preeclamptic
women.11,9 A thorough physical examination and lab-
oratory testing are the priorities. Fetal assessment may
include a nonstress test and/or a biophysical profile. If
the patient is eventually monitored on an outpatient ba-
sis, fetal surveillance may be carried out on a weekly or
twice-weekly basis. The nurse also teaches and/or re-
views with the patient the technique for self-monitoring
of fetal movement.
Although obvious to many nurses as taught in most
nursing education programs, it is important that BP be
assessed properly while using an appropriately sized
cuff. Mercury sphygmomanometers are best, though au-
tomated devices may be used if properly calibrated. It
is recommended that patients be allowed to rest for
at least 10 minutes before BP evaluation, and the BP
should be evaluated with the patient’s arm supported
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at the level of the heart.9,36,37 This is emphasized be-
cause vital signs are often assessed immediately upon
patient arrival to either an inpatient or outpatient set-
ting, and the arm with the cuff is often in a “hanging”
position. Inaccurate BP assessment may lead to unnec-
essary further evaluation and failure to diagnose and
intervene when hypertension is actually present.
Nurses have often assessed outpatient BP with the
patient in a left lateral side lying position on an exami-
nation table if the initial BP is elevated. This is no longer
recommended, as the cuff is higher than the left ventri-
cle in this position and gives a falsely low reading.3,38
However, in the inpatient setting, the BP may be as-
sessed either in the sitting or left lateral recumbent po-
sition with the patient’s cuffed arm at heart level.9
Because exercise, nicotine, and caffeine may tran-
siently increase BP, it should not be assessed within
60 minutes of exercise, smoking, or caffeine ingestion.
Also, it should be noted that evaluation of BP in a
cool room (54◦ F), or while the patient is talking, may
increase the BP by as much as 8 to 15 mm Hg.37,39 Pain
and/or anxiety may also cause intermittent increase in
BP.
In the past, obstetric providers considered a rise of 30
mm Hg systolic blood pressure (“SBP”) or 15 mm Hg di-
astolic blood pressure (“DBP”) as “hypertension indica-
tive of preeclampsia.”9 This rule is not a part of the crite-
ria published by The Working Group11 [nor a part of the
current (ACOG) diagnostic criteria], though the group
consensus is that such rises in either SBP or DBP “war-
rant close observation, especially if proteinuria and hy-
peruricemia are also present.” It should be emphasized
that women with preeclampsia may exhibit a range
of symptoms from minor BP elevation to multisystem
organ dysfunction.7 Care providers should be highly
suspicious of atypical manifestations of preeclampsia
as well, regardless of gestational age or number of
days postpartum at the time of presentation.35 The goal
should be for preeclampsia to be “overdiagnosed” with
the ultimate goal of preventing maternal and perinatal
morbidity and mortality.11 Thus, caregivers need to be
aware that preeclampsia may present as hypertension
without proteinuria, and vice versa.35
Hyperuricemia is defined by the Working Group11
as uric acid at least 6 mg/dL, whereas proteinuria is
defined as at least 0.3 g of protein in a 24-hour collec-
tion. This usually correlates with at least 1 + protein-
uria on random dipstick assessment. However, there is
evidence that accuracy of dipstick urinalysis in diagnos-
ing significant proteinuria is poor, and thus of limited
utility.40 It is recommended that a 24-hour urine sam-
ple be collected if at all possible.11 This test certainly
is subjected to limitations. The urine requires refriger-
ation and collection is time consuming. Many patients
July/September 2011
perform their own collections at home. If collected in-
correctly, the results may be inaccurate and potentially
misleading.
More recently researchers report using a spot
protein/creatinine ratio as a diagnostic test for
preeclampsia instead of the 24-hour protein.41 This test
has been well studied and used outside of pregnancy42
and requires only a single 10 mL of urine sample. Us-
ing a cutoff value of more than 0.3 g/mmol correlated
well to the recommended 24-hour urine protein cutoff
value of more than 0.3 g.41 Furthermore research is rec-
ommended to determine how this test could be used
for the diagnosis of significant proteinuria in pregnancy
and how the values compare against maternal and fetal
morbidity secondary to preeclampsia.41,42
Other laboratory parameters that should be as-
sessed in pregnant women presenting with hyperten-
sion after 20 weeks are hemoglobin and hematocrit,
platelet count, serum creatinine, serum uric acid, serum
transaminase levels, and for women with severe dis-
ease; serum albumin, lactic acid dehydrogenase (LDH),
blood smear, and coagulation profile. In addition to
making an initial diagnosis of preeclampsia, laboratory
evaluation may help with the assessment of possible
worsening disease.11
Although the conventional diagnosis of preeclampsia
is the presence of hypertension after 20 weeks gesta-
tion with proteinuria, the diagnosis may be made even if
proteinuria is absent. Similarly, women with preeclamp-
sia may have evidence of systemic disease even if BP
elevation is minimal.11 Nurses must be aware of the data
and latest recommendations to make a full and accurate
nursing assessment.
Nursing management
Nursing care of the patient with preeclampsia involves
all aspects of the nursing process from assessment to in-
tervention and follow-up. With a thorough understand-
ing of the latest evidence in management of preeclamp-
sia, nurses will be able to provide optimal advocacy and
care for their patients.
The long-held principle that delivery is the only
cure for preeclampsia prevails. Because the underly-
ing pathophysiologic principles are still not well under-
stood, it follows that effective therapies to target the
actual disease are not available. Thus, interventions are
currently designed to either deliver the fetus or make
sure the mother and fetus are safe to continue the preg-
nancy while allowing time for fetal lung maturity to
occur.3,43
The risk of abruptio placentae in women with hy-
pertension in pregnancy is increased.9,10 Furthermore,
eclampsia, the development of new-onset grand mal
seizures in a patient with preeclampsia, is a mater-
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nal complication to be avoided if at all possible. Al-
though these major maternal-fetal complications must
be avoided, efforts at predicting which patient will de-
velop these serious complications have been unsatisfac-
tory. In a recent study, Witlin et al44 evaluated clinical
presentation and laboratory variables, which may be
predictive of either abruption or eclampsia in women
with severe preeclampsia. Neither the extent of protein-
uria or BP elevation was predictive of either of these
serious complications. The investigators noted that ex-
pectant management of severe preeclampsia in their
tertiary care institution has not been associated with
an increase in the frequency of abruption. Although
thrombocytopenia was associated with abruption of the
placenta, it appears to be sequellae of the resultant co-
agulopathy after the abruption rather than a predictor
of placental abruption.
MANAGEMENT
Magnesium sulfate
The chief goals of management in preeclampsia dur-
ing labor and delivery are prevention of seizures and
control of hypertension.9 Magnesium sulfate has been
given to preeclamptic women for years for the purpose
of seizure prevention. Until recently, there was little evi-
dence to support this practice. The international Magpie
Trial,45 which enrolled more than 10 000 women, was
designed to evaluate whether women and/or their chil-
dren are better off when given magnesium sulfate. The
authors45 concluded that use of magnesium sulfate re-
duces the risk of eclampsia by 50% without significant
short-term adverse events for either the mother or the
infant.
Like preeclampsia, the cause of eclamptic seizures
remains unknown. Cerebral vasospasm with resul-
tant ischemia has been proposed as the main cause
of eclampsia. Thus, nimodipine, a calcium channel
blocker known to cause cerebral vasodilation, has
been compared to magnesium sulfate for eclampsia
prevention. Magnesium sulfate was found more ef-
fective for seizure prophylaxis in women with severe
preeclampsia.46
Phenytoin and other antiepileptic drugs have been
evaluated as modes of seizure prevention in women
with preeclampsia. The largest of these studies con-
ducted in the United States provided clear evidence
that magnesium sulfate is “superior” to phenytoin for
the prevention of eclamptic seizures.47 This trial was
yet one more piece of evidence to reinforce the con-
cept that, unless other therapies can show improve-
ment in eclampsia prevention, magnesium should be
considered as the standard of care.46 The use of magne-
sium sulfate in women with mild preeclampsia or mild
www.jpnnjournal.com 249
gestational hypertension remains controversial, al-
though clearly this is the standard for peripartum
women with severe preeclampsia.11
Caution should be exercised with the use of magne-
sium sulfate, as it is excreted by the kidneys, and thus
is considered hazardous for use in women with severe
renal failure.11 In addition to the routine assessments of
deep tendon reflexes, respiratory rate/effort, and breath
sounds, hourly urine output assessment is strongly rec-
ommended for patients receiving magnesium sulfate.
Interestingly, magnesium sulfate has been found to
reduce rates of cerebral palsy in women at risk of deliv-
ering preterm infants at less than 34 weeks of gestation48
ANTIHYPERTENSIVE THERAPY
The purpose of acute treatment for severe hypertension
is stroke prevention. Some experts recommend treat-
ment with antihypertensive agents for persistent DBP
at least 105 mm Hg. Others advise not administering
medications until DBP reaches 110 mm Hg.5,21 Antihy-
pertensive therapy should be considered if the patient
exhibits signs of end-organ damage such as nephropa-
thy, left ventricular hypertrophy, or severe retinopathy.
A hypertensive emergency, requiring management in
an intensive care unit, would be defined as persistent
BP higher than 240/140 mm Hg. As with all acute an-
tihypertensive therapy in pregnancy, the goal should
not be to reduce BP to the normal range. Rather, the
goal should be to decrease the diastolic pressure to
“just below 100 mm Hg” because of the possible fetal
effects resulting from a rapid decrease in uteroplacental
perfusion.49
Hydralazine is a peripheral arteriolar vasodilator
which, up until recently, was the most commonly used
antihypertensive drug in the setting of acute hyperten-
sion in pregnancy.5,49 As with all medications, nurses
must be especially aware of the length of time it takes
from when the medication is administered until the
first dose takes effect. The onset of action with hy-
dralazine is gradual with a peak at 20 minutes. It is
possible that rapid or excessive decrease in maternal
BP may decrease placental perfusion and lead to ad-
verse maternal-fetal sequelae. When nurses incorporate
the knowledge of the drug’s pharmacokinetics, they will
be able to avoid the common mistake of administering
doses of the drug too close together.
In a meta-analysis by Magee et al,50 hydralazine was
shown to have more maternal and fetal side effects than
were seen with other antihypertensives, specifically la-
betalol and nifedipine. Thus, many perinatal centers
have changed protocols to move labetalol to the first-
line antihypertensive agent with hydralazine as a sec-
ond choice.
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Labetalol is commonly used in pregnancy, and is
now the most commonly used agent in the event of
acute hypertension.49 The onset of action begins at
5 minutes with a peak effect at 10 to 20 minutes. La-
betalol is both an α- and β-blocker, with more β effect
than α. As such, it causes a decrease in the systemic
vascular resistance and decreases the heart rate without
decreasing maternal cardiac output. Labetalol should be
avoided in patients with a history of asthma or conges-
tive heart failure.5
Nifedipine, a calcium channel blocker, is an arterio-
lar vasodilator commonly used in pregnancy. Through
its action of blocking calcium’s entry into the cells (and
considering that calcium must be present for a smooth
muscle contraction to occur), nifedipine reduces the
peripheral vascular resistance through vasodilation.
Because many patients receiving therapy for acute hy-
pertension in pregnancy are also receiving magnesium
sulfate for seizure prophylaxis, consideration must
be given to the risk of neuromuscular blockade in
patients receiving both a calcium channel blocker and
magnesium sulfate.49,5 Although this risk is minimal, an
awareness of the cellular-level physiology involved is
important.
Sodium nitroprusside is reserved for the rare cases
of acute hypertensive emergency when the first line
agents have failed. This drug has a very rapid onset
of action and peak effect. When using this medication,
the patient must be in an intensive care unit setting.
The drug metabolizes to cyanide, thus, if used on a
pregnant woman, the entire care team should all be
cognizant of the cyanide risk to the fetus, though this
concern remains unproven.49
Recurrence risk and long-term health implications
of preeclampsia
Although preeclampsia is thought to be a “disease of
primigravidas,” it is more than 3 times more common in
multiparous women with a history of the disease than
in nulliparas.51 The risk of recurrence varies with the
time of onset of symptoms and severity of the disease
process experienced in the previous preeclamptic preg-
nancy. Mild preeclampsia diagnoses near term have a
low incidence of recurrence in future pregnancies.52 In
contrast, patients with severe preeclampsia, particularly
if occurring in the second trimester, are at high risk for
recurrent preeclampsia in subsequent pregnancies.53
It has been well known for quite some time that
women who develop gestational diabetes are at risk for
eventual development of adult-onset (type II) diabetes.
More recently, it has been established that preeclamp-
sia is a risk factor for development of cardiovascu-
lar disease. This evidence has emerged on the basis
of the known link between endothelial and vascular
July/September 2011
dysfunction common in both preeclampsia and
atherosclerosis. Furthermore, there is now research that
suggests that fetuses who are products of preeclamp-
tic pregnancies have, themselves, an increased risk of
cardiovascular disease.4,5
Nurses are in a unique position to impact the fu-
ture health of both mothers and babies affected by
preeclampsia. Nurses should discuss with their pa-
tients the diagnosis of preeclampsia as a bona fide
cardiovascular risk. Because pregnant women develop
preeclampsia during their childbearing years, they are
generally young enough that cardiovascular disease has
not yet been diagnosed. This offers nurses a chance to
partner with their patients not only to develop lifestyle
modification strategies, but also to institute “early and
aggressive screening for hypertension.”4 A tailored plan
for risk reduction, initiated by nurses armed with
strong assessment, counseling and advocacy skills,
affords the patient an opportunity to optimize lifetime
health.
CONCLUSION
Hypertension in pregnancy is a serious problem, com-
plicating up to 6% to 8% of pregnancies.5 As out-
lined before, the causes of preeclampsia are unknown,
whereas study on the associated pathophysiology, op-
timal assessment, diagnosis, and treatment modalities
continue. Because nurses are usually on the front line
of the healthcare system, they are in the strategic posi-
tion to make significant contributions to the current and
long-term health of mothers and babies. Thus, nurses
must continue with ongoing study and evaluation of
the latest information on preeclampsia to be effective
in their roles as caregivers, advocates, and patient edu-
cators.
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