Download Hypertensive Disorders of Pregnancy

PRINCIPLES & PRACTICE
Hypertensive Disorders of Pregnancy
Rosalind M. Peters and John M. Flack
Hypertensive disorders occur in 6% to 8% of all
pregnancies, are the second leading cause of maternal death, and contribute to significant neonatal morbidity and mortality. This is a problem not only in
inpatient settings, as ambulatory and home-care nurses are increasingly being called upon to monitor
women who are at high risk and may have hypertensive disorders. To prevent hypertension-induced problems in pregnant women, nurses must have strong
assessment, advocacy, and counseling skills. Nurses
also must provide care based on the latest national
standards as described in this article. JOGNN, 33,
209-220; 2004. DOI: 10.1177/0884217504262970
Keywords: Eclampsia—Gestational hypertension—Preeclampsia—Pregnancy-induced hypertension
Accepted: February 2003; updated December 2003
Hypertensive disorders of pregnancy are the second leading cause of maternal death in the United
States. They also contribute significantly to stillbirths and neonatal morbidity and mortality
(National High Blood Pressure Education Program
Working Group [NHBPEP], 2000). Hypertensive
disorders can result in cerebral hemorrhage, disseminated intravascular coagulation (DIC), hepatic failure, acute renal failure, and abruptio placentae
(Flack, Peters, Mehra, & Nassar, 2002). The pathogenesis, classification, and treatment of high blood
pressure (BP) in pregnancy differ from nonpregnant
care, especially as there are two patients to consider
simultaneously and because severe complications
can occur rapidly within hours of the initial diagno-
March/April 2004
sis. In addition, the risk of serious sequelae of
preeclampsia can persist up to 5 days postpartum.
Thus, nurses working in outpatient, home care,
and acute care settings must be vigilant when assessing pregnant women so that hypertensive problems
are identified early and treated promptly. As patient
advocates who ensure optimal maternal and neonatal outcomes, nurses must have a full understanding
of (a) the need for accurate blood pressure measurements to ensure accurate diagnosis, (b) the differences associated with the four major categories of
high blood pressure in pregnancy, (c) the physiological changes of pregnancy that affect blood pressure,
(d) the pathophysiology of preeclampsia and chronic hypertension in pregnancy, (e) methods of identifying and preventing preeclampsia, (f) appropriate
management of hypertensive disorders of pregnancy,
and (g) the clinical implications.
Blood Pressure Measurement Accuracy
Elevated blood pressure may occur in pregnancy
secondary to a prepregnancy condition or from two
pregnancy-specific disorders: preeclampsia and gestational hypertension. The impact of high blood
pressure on pregnancy is related more to the underlying pathology of the condition than to the actual
elevation in pressure. Thus, the optimal management of hypertensive disorders in pregnancy begins
with an accurate diagnosis, as the treatment and
prognosis vary significantly based on the etiology of
the hypertension. Accurate diagnosis begins with
accurate measurement of blood pressure. Therefore,
nurses must know the procedures required to ensure
JOGNN 209
accuracy and make delegation decisions based on this
knowledge.
TABLE 1
Classification of High Blood Pressure in Pregnancy
Blood Pressure Protocol
There has been controversy about how to measure BP
(e.g., position, sound for diastolic pressure). Blood pressure should be measured with the woman seated and her
arm at heart level, using an appropriate-sized cuff. It is no
longer recommended to measure BP with a woman lying
on her left side. In that position, the cuff is higher than the
left ventricle, resulting in reduced hydrostatic pressure.
This gives an inaccurately low reading, often reduced by
as much as 10 to 14 mm Hg (Barron & Lindheimer,
1995). Diastolic pressure should be reported as the fifth
Korotkoff phase (K5, disappearance of sound), not the
fourth phase (K4, “muffling” of sound) (NHBPEP, 2000).
Previous literature indicated that there was a significant
difference between K4 and K5 in pregnant women; however, later evidence has shown that K5 more closely
reflects true diastolic pressure (Blank, Helseth, Pickering,
NHBPEP Classification
I. Chronic
hypertension
II. PreeclampsiaEclampsia
III. Preeclampsia
superimposed
on chronic
HTN
IV. Gestational
hypertension
Hypertension prior to conception, or
before 20th week gestation
Preeclampsia—systemic disease with
hypertension accompanied by
proteinuria after 20th week of
gestation
Eclampsia—convulsive stage
of the disease
Hypertensive women who develop new
onset proteinuria; proteinuria before
20th week gestation; or sudden
uncontrolled hypertension
High blood pressure detected for the
first time after mid-pregnancy, without
proteinuria; diagnosis is made
postpartum
Source. NHBPEP (2000).
B
lood pressure measurement accuracy is vital,
and care should be taken when this task is
delegated to unlicensed personnel.
West, & August, 1994; Brown, Buddle, Farrell, Davis, &
Jones, 1998; Johenning & Barron, 1992).
Accuracy of BP measurement is a significant concern in
pregnancy. Conventional BP measurement is subject to a
variety of errors arising from the patient, the person taking the measurement, and/or the environment. To reduce
these errors, 24-hour ambulatory monitoring may be used
(Aitken & Addison, 1996; Myers, 1999). The ambulatory method gives an average BP reading for 24 hours as
determined by multiple readings taken during a patient’s
normal home and work routine. Some studies have found
ambulatory monitoring to be a more sensitive predictor of
progression to severe hypertension in women whose BP
measurement in the clinic is higher than 140/90 mm Hg
(Penny et al., 1998). Although there has been an increased
use of ambulatory monitoring in pregnancy, its efficacy
and cost-effectiveness have not been established (Lindheimer & Akbari, 2000).
Classification of Hypertension
A number of different classification schemes and terminologies have been used to describe high BP in pregnancy (e.g., American College of Obstetricians and Gyne-
210 JOGNN
Note. Hypertension ≥ systolic pressure ≥ 140 mm Hg; diastolic pressure ≥ 90 mm Hg.
cologists [ACOG], the Canadian Hypertension Society,
the U.S. National High Blood Pressure Education Program [NHBPEP]). Previous ACOG terminology distinguished between two disorders: chronic hypertension and
pregnancy-induced hypertension (PIH), with PIH having
different subsets depending on end-organ involvement
(ACOG, 1996a, 1996b). The NHBPEP (2000) advocates
discarding the term pregnancy-induced hypertension
because it does not differentiate between gestational
hypertension, a relatively benign disorder, and the more
serious preeclampsia. The NHBPEP recommends the use
of four categories: chronic hypertension, preeclampsiaeclampsia, preeclampsia superimposed on chronic hypertension, and gestational (transient/chronic) hypertension
(NHBPEP, 2000) (see Table 1).
The NHBPEP justifies its classification system based on
“best-evidence” and consensus data, indicating that some
criteria used by other groups are not justified, given the
currently available data. Within the NHBPEP system,
T
he term pregnancy-induced hypertension
should be discarded because it does not
differentiate between gestational hypertension
and the more serious preeclampsia.
Volume 33, Number 2
chronic hypertension is defined as hypertension that was
either present before conception or detected before the
20th week of gestation and did not resolve in the early
postpartum. Chronic hypertension of pregnancy is further
defined as including women with systolic blood pressure
(SBP) of 140 mm Hg or higher, or diastolic blood pressure
(DBP) above 90 mm Hg or higher.
Preeclampsia-eclampsia is a pregnancy-specific systemic syndrome. The diagnosis of preeclampsia is determined by the presence of hypertension, occurring after the
20th week of gestation, accompanied by proteinuria.
Preeclampsia also may be diagnosed without proteinuria
if there are other systemic symptoms such as visual
changes, headache, abdominal pain, or abnormal laboratory values (NHBPEP, 2000). Eclampsia is the convulsive
phase of preeclampsia, when the seizures cannot be attributed to other causes. Preeclampsia superimposed on
chronic hypertension is the disorder most often associated with severe maternal and fetal complications, and the
prognosis is much worse than for either condition alone
(Barron & Lindheimer, 1995; NHBPEP, 2000). Superimposed preeclampsia hypertension is a strong consideration (a) in women who were hypertensive before the 20th
week of gestation but have new onset of proteinuria, (b)
in women with both hypertension and proteinuria before
20 weeks gestation, (c) in women with previously controlled hypertension who have a sudden increase in BP,
and (d) in women with thrombocytopenia (< 100,000
cells/mm3) and elevated hepatic enzymes (alanine aminotransferase [ALT] or aspartate aminotransferase [AST])
(NHBPEP, 2000).
The term gestational hypertension may be used in
pregnancy until a more specific diagnosis can be made,
which is often not until the postpartum. Gestational
hypertension may be transient or chronic in nature. Transient hypertension of pregnancy refers to an elevated
blood pressure that occurs without proteinuria late in
pregnancy or in the early puerperium, but returns to normal levels by 12 weeks postpartum. Chronic gestational
hypertension is used to describe a woman without evidence of preeclampsia whose blood pressure remains elevated beyond 12 weeks postpartum. Gestational hypertension is a relatively benign disorder with good
outcomes, which is one reason the NHBPEP eliminated
the term pregnancy-induced hypertension. There are
important differences in the hypertension of preeclampsia
and either transient or chronic gestational hypertension
that reflect the underlying pathogenesis of the disorders.
eral resistance decreases by 25% due to a combination of
factors such as (a) the development of vessel resistance to
the pressor effects of angiotensin II (Ito, Nakamura,
Yoshimura, Koyama, & Okamura, 1992); (b) increased
prostaglandin synthesis, with an increase in the potent
vasodilator, prostacyclin; (c) increased nitric oxide synthase; and (d) increased production of the endotheliumderived relaxing factor (Poston, 1996; Sladek, Magness,
& Conrad, 1997). There is a 50% rise in total blood volume by the end of the 2nd trimester, and cardiac output
increases in the 1st trimester, peaking at 35% to 50%
above nonpregnant values (Poppas et al., 1997; van
Oppen, Stigter, & Bruinse, 1996). Changes also occur
within the renal system, including increased renal blood
flow, a significant increase in the glomerular filtration
rate, and activation of the renin-aldosterone system,
resulting in a falling BP (Sturgiss, Wilkinson, & Davison,
1996).
In uncomplicated pregnancy, the diastolic pressure
drops to an average of 10 mm Hg below nonpregnant values by midpregnancy, then slowly approaches nongravid
levels in the 3rd trimester (Barron & Lindheimer, 1995).
Therefore, a high level of suspicion should occur for
women with a DBP of 75 mm Hg, or SBP of 120 in midpregnancy, or 85 mm Hg diastolic or 130 mm Hg systolic
in later pregnancy (Lindheimer & Akbari, 2000). Women
with preexisting hypertension tend to have even greater
decreases in their BP in early pregnancy, and their “normal” rise in the 3rd trimester may be misdiagnosed as
preeclampsia (Kaplan, 1998).
Blood pressure in preeclampsia is characterized by a
reversal of the vasodilatory characteristics of uncomplicated pregnancy, resulting in a marked increase in peripheral resistance (Visser & Wallenburg, 1991). Blood pressure also behaves differently in women with
preeclampsia, who can have highly labile pressures and
could experience a flattening or reversal of normal circadian BP rhythms, with their highest values recorded at
night (Lindheimer & Akbari, 2000). Although the precise
etiology of preeclampsia is unknown, it is thought to be
caused by disruptions within the placenta, possibly mediated by immunological mechanisms and occurring in
women with a genetic predisposition (Brown & Whitworth, 1999). Diagnosis and management of preeclampsia require an understanding of its underlying pathogenic
features.
Blood Pressure in Uncomplicated
Pregnancy and Preeclampsia
Preeclampsia is a pregnancy-specific syndrome with a
clinical continuum ranging from mild to severe forms of
the condition (NHBPEP, 2000). Preeclampsia is more
than just a hypertensive problem; it is a systemic disorder
with both maternal and fetal manifestations. Preeclamp-
A number of changes occur in uncomplicated pregnancy that cause it to be a markedly vasodilated state. Periph-
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Pathophysiology of Preeclampsia
JOGNN 211
sia may involve multiple organs, and many of its nonhypertensive complications can be life-threatening, even
when blood pressure elevations are mild. The pathophysiology of preeclampsia can be divided into two stages:
alterations in placental perfusion (stage 1) and the maternal syndrome (stage 2) (Roberts, Pearson, Cutler, & Lindheimer, 2003). The problems seen with preeclampsia
begin with the placental changes of stage 1. The endovascular trophoblast cells of the placenta are supposed to
transform spiral arteries in the uterus to accommodate
increased blood flow. In preeclampsia, the arterial transformation is incomplete and women with the condition
have a distinctive lesion termed acute atherosis, as well as
a greater degree of placental infarction than is seen in normotensive gravidas, both of which can lead to decreased
placental perfusion and placental hypoxia (NHBPEP,
2000). This supports the hypothesis that placental hypoxemia is the proximate cause of preeclampsia (Conrad &
Benyo, 1997; Roberts et al., 2003).
Stage 2, the maternal syndrome, begins when plasma
volume is reduced, as compared to an uncomplicated
pregnancy, with decreased blood flow to organs other
than the placenta resulting in hemoconcentration, hemorrhage, and necrosis (Roberts et al., 2003). Immunological
alterations occur with an increased level of inflammatory
cytokines in the placenta and maternal circulation. The
vasculature changes noted in preeclampsia appear to be
due to alterations in the ratio of circulating thromboxane
and prostacyclins, with an increase in the vasoconstrictive
thromboxane (Baker, Davidge, Barankiewicz, & Roberts,
1996; Mills et al., 1999), increased sensitivity to pressor
substances (e.g., angiotensin II and endothelin), decreased
production of endothelium relaxing factor, and cytokineproduced endothelial cell damage (Baylis, Beinder, Suto,
& August, 1998). The coagulation system is activated in
preeclampsia, and thrombocytopenia occurs, possibly due
to increased platelet aggregation and deposition at sites of
endothelial damage (Ballegeer et al., 1992).
Changes in the kidney include a swelling of the
glomerular endothelial cell cytoplasm, causing a characteristic lesion, glomerular endotheliosis, which correlates
with proteinuria (Lockwood & Paidas, 2000). Both the
renal blood flow and glomerular filtration rate are
decreased in preeclampsia. Uric acid clearance and renal
calcium are affected, resulting in hypocalciuria and elevated serum urate levels (NHBPEP, 2000).
Liver damage may be mild, with elevated serum
enzymes (aminotransferase and lactate dehydrogenase),
or may progress to encompass the HELLP syndrome
(hemolysis, elevated liver enzymes, low platelets). In
preeclampsia there is an increase in microvascular fat deposition within the liver, which directly correlates with
plasma uric acid levels, and inversely correlates with
platelet counts (Minakami et al., 1998). Expansion of the
212 JOGNN
liver parenchyma secondary to fat deposition is postulated as one cause of epigastric pain seen in severe
preeclampsia.
Convulsions mark the eclamptic phase of preeclampsia
and indicate central nervous system involvement; seizures
are no longer believed to result only from hypertensive
encephalopathy, as convulsions have occurred in women
with mild elevations of pressure (Sibai, 1996). Instead,
vasoconstriction, resulting in widespread microvascular
cerebral changes and ischemia, is believed to be the major
factor causing the seizure disorder (Lockwood & Paidas,
2000).
Chronic Hypertension Versus Preeclampsia
Differentiating between chronic hypertension and
preeclampsia is especially important, as there are significant differences in their management as well as in the
implications for fetal viability and future pregnancies. In
chronic hypertension, the elevated blood pressure is the
major problem, whereas in preeclampsia, the elevated
blood pressure is just one symptom of an underlying multiorgan disorder. When there is uncertainty about the
underlying cause, it is recommended that preeclampsia be
diagnosed and treatment instituted immediately because
preeclampsia can progress rapidly (NHBPEP, 2000).
Many of the pathophysiological changes of preeclampsia occur before clinical symptoms are present. In addition, because of the multitude of organs affected, the clinical presentation of preeclampsia may manifest in a wide
variety of ways. As a result, there is no single test or group
of tests that definitively detect preeclampsia at an early
stage (Dekker & Sibai, 2001; Masse et al., 1993). Laboratory tests (e.g., serum creatinine, hepatic enzymes,
platelet counts) are designed primarily to distinguish
between preeclampsia and chronic or transient hypertension, as well as to serve as a marker for the severity of
preeclampsia when it is present (see Table 2). Edema, no
longer included as a cardinal symptom of preeclampsia,
occurs in too many uncomplicated pregnancies to have
predictive value.
Identifying and Preventing Preeclampsia
Given that no test is reliable enough to be used as a
routine screening tool for predicting preeclampsia (Witlin
& Sibai, 1997), clinical diagnostic skills become vitally
important for early identification of the condition. Nurses should carefully monitor women who are considered to
be at greater risk for developing preeclampsia. The risk
factors for preeclampsia include age older than 40 years,
nulliparity, African American ethnicity, presence of preexisting disease (e.g., chronic hypertension, renal disease,
diabetes mellitus), multifetal pregnancy, family history of
Volume 33, Number 2
TABLE 2
Clinical Manifestations of Preeclampsia
Signs of Mild Preeclampsia
1. Mild elevations in BP
Systolic ≥ 140 mm Hg or
Diastolic ≥ 90
2. Proteinuria > 2.0 g/24 hours
(2+ or 3+ on dipstick)
(proteinuria should occur
for the first time in pregnancy)
3. Increased serum creatinine
(> 1.2 mg/dL unless known
to be previously elevated)
4. Normal platelet count
5. Normal liver enzymes
6. No maternal symptoms
Signs of Preeclampsia
Superimposed on Chronic Hypertension
1. In women with hypertension and
no proteinuria early in pregnancy
(< 20 weeks) New onset proteinuria,
defined as urinary excretion of
> 3 g/24 hours
2. Women with hypertension and
proteinuria before 20 weeks
gestation
3. Sudden increase in proteinuria
4. Sudden increase in blood pressure
in woman whose blood pressure
had been previously controlled
5. Thrombocytopenia
6. An increase in ALT or AST to
abnormal levels
pregnancy-induced hypertension, and previous preeclampsia if a multipara (Flack et al., 2002). Obese
women (body mass index of 29 or higher) are 3 times
more likely to develop preeclampsia than nonobese
women (Dekker & Sibai, 2001).
Women at high risk should have laboratory tests (e.g.,
hematocrit, hemoglobin, platelet count, liver enzymes,
and serum creatinine and uric acid levels) early in pregnancy to provide baseline data and should have frequent
prenatal care to assess both maternal and fetal progress
(NHBPEP, 2000). Increasing attention is being paid to
uric acid as an important early predictor of preeclampsia
because increased urate concentrations have been found
to coincide with increasing blood pressure, while preceding proteinuria (Dekker & Sibai, 2001).
Sodium Restriction/Diuretic Use
Prevention of preeclampsia has been hampered by the
lack of full understanding of the pathogenic mechanisms
involved. Empiric approaches have been attempted with
little overall success. Sodium restriction and diuretic therapy were tested in an attempt to control preeclamptic
hypertension. However, analysis revealed that the interventions, although successful in reducing edema, did not
prevent or reduce proteinuric hypertension (Collins,
Yusuf, & Peto, 1985). Concern was raised that this prophylaxis, by lowering blood pressure and reducing
edema, might mask signs of preeclampsia without altering
the underlying disease. At the same time, lowering the
March/April 2004
Signs of Severe Preeclampsia
(one or more of the following should be present)
1. Elevated blood pressure: Absolute value
of: Systolic ≥ 160 mm Hg or
diastolic ≥ 110 mm Hg - Or relative value
of a rise of 30 mm Hg systolic or
15 mm Hg diastolic
2. Proteinuria, > 5.0 gm/24 hours
(3+ or 4+ on dipstick)
3. Increasing serum creatinine (> 2 mg/dL)
4. Rapid decreases in platelet count
(< 100,000/mm3 and/or evidence of
microangiopathic hemolytic anemia
(with increased lactic acid dehydrogenase)
5. Oliguria < 500 ml/24 hours
6. Cerebral symptoms: persistent headache,
visual changes, altered consciousness
7. Persistent epigastric or right upper
quadrant pain
8. Intrauterine growth restriction and/or
oligohydramnios
blood pressure increases the possibility of inhibited fetal
growth by reducing uteroplacental blood flow. Therefore,
the risk-benefit considerations contraindicate the use of
diuretics and sodium restriction as a prophylactic to prevent preeclamptic hypertension (Barron & Lindheimer,
1995).
Calcium Supplements
Calcium supplementation to prevent preeclampsia was
attempted, on the basis that hypocalciuria occurred with
the disease. Although initial studies looked promising, a
large randomized clinical trial failed to detect any benefits
of calcium supplementation in preventing preeclampsia,
delaying its onset, or reducing its severity in low-risk
women. Calcium supplementation may have some benefit
in women with a low calcium intake (Dekker & Sibai,
2001; Levine et al., 1997) but is not recommended as a
general preventive measure.
Low-Dose Aspirin
Prophylactic low-dose aspirin therapy was also evaluated. Its usage was based on the principle that aspirin
would inhibit synthesis of thromboxane while sparing
prostacyclin production. Again, initial results seemed
promising, but a review of several large randomized trials
found that aspirin failed to reduce the incidence of
preeclampsia and did not improve maternal or fetal outcomes (NHBPEP, 2000). An additional study with highrisk women (e.g., diabetics) also failed to show any bene-
JOGNN 213
fit from low-dose aspirin prophylaxis (Caritis et al.,
1998). A recent Cochrane review of the effectiveness and
safety of antiplatelet agents, predominantly aspirin, concluded that despite small overall benefits, including a
15% reduction in preeclampsia, a number of questions
remain. As a result, there is insufficient evidence to make
a clear recommendation for the use of low-dose aspirin in
the prevention of preeclampsia (Knight, Duley, Henderson-Smart, & King, 2001).
Prophylactic Antihypertensive Therapy
Antihypertensive medications were also evaluated as a
prophylaxis on the basis of the belief that early treatment
of hypertension could prevent or delay the other manifestations of preeclampsia. However, there is no evidence to
indicate that elevated blood pressure triggers or causes the
uteroplacental, cerebral, renal, hepatic, and coagulation
pathogenic changes seen in preeclampsia. Studies found
no evidence to support that prophylactic antihypertensives prevented preeclampsia or improved fetal outcomes
(Plouin et al., 1990; Sibai, Mabie, Shamsa, Villar, &
Anderson, 1990; von Dadelszen et al., 2000).
Management of Preeclampsia
Delivery
Delivery of the fetus and placenta is the only “cure” for
preeclampsia. There are little data to suggest that any
therapy alters the underlying pathophysiology. Therefore,
all other interventions are designed to safeguard the
mother while allowing time for fetal maturity. Although
delivery cures preeclampsia, its effect is not immediate
and women remain at risk of continuing problems,
including eclampsia, as long as 5 days postpartum (Flack
et al., 2002). Careful postpartum follow-up is vitally
important as hypertension and proteinuria may persist for
weeks (NHBPEP, 2000).
Careful Monitoring
Initial assessment as an inpatient is recommended for
all women with new-onset preeclampsia (NHBPEP,
2000). The assessment should include careful assessment
of each woman’s complaints, a physical examination, and
laboratory tests. Assessment of the fetus should include
nonstress testing, a biophysical profile, and assessment of
fetal activity.
Hospitalization is frequently advised to facilitate
restricted activity. Close monitoring of mother and fetus
can detect early signs of advancing preeclampsia and
expedite intervention and delivery as indicated by advancing disease. Restricted activity, often bed rest, is consid-
214 JOGNN
ered a “usual and reasonable” recommendation, even
though its efficacy has not been established (Brown,
1990). Preliminary results of home care and outpatient
management have been encouraging for a select group of
patients with mild preeclampsia earlier in pregnancy (Barton, Olson, & Sibai, 1994; Crowther, Bouwmeester, &
Ashurst, 1992; Tuffnell et al., 1992). Conservative monitoring has been shown to reduce neonatal morbidity
through prolonged gestation, but many physicians do not
recommend this treatment for women with severe
preeclampsia who are far from their due dates. Those
women are at very high risk for eclampsia, renal failure,
ruptured liver, and cerebral hemorrhage with poor fetal
outcomes, and may be advised to terminate the pregnancy with early delivery of the fetus. However, terminating
a pregnancy is the source of controversy that is not currently resolved (Lindheimer & Akbari, 2000).
Prevention of Eclamptic Seizures
Preventing convulsions is a major concern in the management of preecalmpsia, and antiseizure medication may
be initiated. Two randomized trials have shown the benefit of magnesium sulfate in reducing the incidence of
eclampsia in women with severe preeclampsia (Coetzee,
Dommisse, & Anthony, 1998; Lucas, Leveno, & Cunningham, 1995). The benefits of drug therapy in mild
preeclampsia are unknown. There is conclusive evidence
that magnesium sulfate is the drug preferred for use in
preventing recurrent seizures. Magnesium sulfate has
been proven safer and more effective than diazepam or
phenytoin (Collaborative Eclampsia Group, 1995; Lucas
et al., 1995). However, magnesium sulfate in conjunction
with calcium blockers can result in profound hypotension, and women treated with both drugs need to be carefully assessed. In addition, magnesium sulfate is hazardous for women with severe renal failure and lower
dosages are required (NHBPEP, 2000).
Control of Blood Pressure
Antihypertensive medications have not been shown to
improve perinatal outcomes in mild to moderate
preeclampsia (140-160/90-110 mm Hg) and should not
be routinely prescribed (NHBPEP, 2000). There is, however, general agreement that aggressive pharmacological
intervention is warranted for blood pressure found in
severe preeclampsia (SBP ≥ 160 mm Hg; DBP ≥ 110 mm
Hg; or rapidly rising blood pressure with changes > 30
mm Hg systolic and > 15 mm Hg diastolic) (NHBPEP,
2000). Some experts will initiate antihypertensive therapy
at a DBP of 105 mm Hg if other risk factors are present,
and in pregnant adolescents treatment may begin at 100
mm Hg DBP (NHBPEP, 2000). The goal of antihyperten-
Volume 33, Number 2
TABLE 3
Results of Laboratory Tests to Be Reported
Normal Results†
Test
Proteinuria
10-100 mg/24 hours
Hemoglobin and hematocrit
Hgb 12-15 gm/100 ml Hmct
37-47/100 ml
0.2-0.5 mg/dl
Serum creatinine
Serum albumin
Uric acid
Platelet count**
Serum transaminase**
(ALT- alanine aminotransferase,
or AST - aspartate
aminotransferase)
Lactic acid dehydrogenase**
4-4.45 gm%
Serum: 3.0-7.5 mg/100 ml
Urine: 0.4-1.0 gm/24 hours
150,000-350,000/mm3
ALT 0-48 IU/L AST 0-36 IU/L
120-340 I.U./L
Results to Be Reported
Increasing levels especially = 3+ dipstick or = 3 g in
24-hour specimen indicates increasing renal involvement
Increasing hemoconcentration is associated with
%preeclampsia and is an indicator of its severity
Abnormal levels (> 1.2 mg/dL) or rising levels, especially
with oliguria
Decreased levels indicates the extent of endothelial leak
Increasing serum levels and decreasing urine levels indicate
reduced kidney function
Significantly decreasing levels, OR absolute counts
< 100,000/mm3
Rising levels indicate severe preeclampsia with hepatic
involvement
Increase indicates presence of hemolysis
** indicates possible HELLP syndrome.
† Fischbach (2000).
sive therapy is to prevent eclampsia and stroke, but the
drug must also be safe for the fetus (see Antihypertensive
Medications in Pregnancy).
Management of Chronic Hypertension
in Pregnancy
Prepregnancy Counseling
Chronic hypertension of pregnancy can be classified as
mild (BP ≥ 140/90) or severe (≥ 180/110) (ACOG, 2001).
Uncomplicated, mild chronic hypertension usually is not
associated with increased maternal or fetal risk. Most of
the increased risk from chronic hypertension is associated
either with severely elevated blood pressures (≥ 180 mm
Hg SBP; ≥ 110 mm Hg DBP) in the 1st trimester (50%
fetal loss and significant maternal mortality) or with
preeclampsia superimposed on the chronic condition
(Sibai et al., 1998). In the best of situations, management
of chronic hypertension in pregnancy begins before conception. Prepregnancy counseling is important, so that
women discontinue antihypertensive medications known
to be embryotoxic (e.g., angiotensin converting enzyme
inhibitors, angiotensin II receptor antagonists) and have
sufficient time to determine their response to a new antihypertensive regimen (Chobanian et al., 2003). Assessment of renal function, by measuring serum creatinine
March/April 2004
and collecting a 24-hour urine specimen for creatinine
clearance and protein concentration, provides important
baseline data that can help differentiate between underlying pathology and onset of preeclampsia in pregnancy.
Antihypertensive Therapy for Chronic
Hypertension
The efficacy of antihypertensive therapy for mild,
chronic hypertension is uncertain (ACOG, 2001). There
is some evidence that antihypertensive medications help
prevent progression to severe hypertension during pregnancy (Sibai, 1996; Sibai et al., 1990). However, two retrospective studies found that these medications did not
reduce the frequency of superimposed preeclampsia,
preterm delivery, or abruptio placentae in treated versus
untreated women (Rey & Couturier, 1994; Sibai et al.,
1990). In addition, there is no evidence that antihypertensive therapy improves neonatal outcomes (NHBPEP,
2000). A concern remains that while it may be beneficial
to the mother to reduce blood pressure, the lower pressure may impair uteroplacental blood flow and affect
fetal growth. The need for antihypertensive drugs is also
questioned in that blood pressure decreases in the first 2
trimesters of pregnancy and women with chronic hypertension may experience an even greater drop. As a result,
it may be possible to taper these women off their medications and prescribe nonpharmacological management
JOGNN 215
with careful monitoring. Antihypertensive therapy should
be reinstituted if blood pressure reaches 150-160 mm Hg
SBP or 100-110 mm Hg DBP (NHBPEP, 2000).
Antihypertensive Medications in Pregnancy
Medication choices in pregnancy are limited because a
number of the antihypertensives are embryotoxic and
there is a lack of extensive randomized clinical trials on
which to base their use (Flack et al., 2002). Very few antihypertensive medications qualify for the Food and Drug
Administration’s Category A grouping. (Category A drugs
are those for which controlled studies have been conducted in humans and the drugs do not demonstrate a risk to
the fetus.) (Lindheimer & Akbari, 2000)
Methyldopa (central adrenergic inhibitor) is the preferred drug for treating chronic hypertension during
pregnancy (ACOG, 2001). Methyldopa controls maternal
blood pressure and has been found to have stable uteroplacental blood flow with good fetal hemodynamics.
Methyldopa’s efficacy has been well established in randomized trials, and the drug has a long history of safe,
effective use for both mother and fetus (Cockburn, Moar,
Ounsted, & Redman, 1982; Kyle & Redman, 1992;
Montan, Anandakumar, Arulkumaran, Ingemarsson, &
Ratnam, 1993; Plouin et al., 1990). The long-term effects
of methyldopa were evaluated in one 7-year prospective
study, which found no adverse effects in the children
exposed to the drug in utero (Cockburn et al., 1982).
Hydralazine has long been the preferred vasodilator
for acute hypertensive crises but is a second-line drug
after methyldopa for treatment of chronic hypertension.
Some authors (Magee, Ornstein, & von Dadelszen, 1999)
have suggested that hydralazine should no longer be the
preferred drug for treatment of acute hypertensive crises,
based on their review of the literature, and instead have
suggested intravenous labetalol or oral nifedipine.
Nifedipine has been used to treat acute hypertensive crises
of pregnancy because of its rapid, albeit unpredictable,
reductions in blood pressure. However, the Food and
Drug Administration has not approved oral nifedipine for
such use. In addition, nifedipine has been associated with
fatal and nonfatal cardiovascular events and is therefore
not recommended for use in hypertensive crises
(NHBPEP, 2000; National Institutes of Health, 1997).
Labetalol, given as an intravenous bolus injection, has
been shown to be an effective drug for treating hypertensive crisis of pregnancy. However, it should not be used in
women with asthma or congestive heart failure. Following the dictum that the medication with the longest
uneventful history in pregnancy should prove the safest,
hydralazine is the drug preferred for use in hypertensive
crises, whereas methyldopa is preferred for treatment of
216 JOGNN
chronic hypertension in pregnancy (Lindheimer &
Akbari, 2000; NHBPEP, 2000).
Antihypertensive Therapy Cautions
During Pregnancy
Angiotensin converting enzyme inhibitors are contraindicated in pregnancy (Chobanian et al., 2003;
NHBPEP, 2000). They are associated with growth restriction, oligohydramnios, irreversible fetal/neonatal renal
failure, and neonatal death (Hanssens, Keirse, Vankelecom, & Van Assche, 1991; Piper, Ray, & Rosa, 1992).
Angiotensin II receptor antagonists are believed to have
similar results as ACE inhibitors and are not recommended in pregnancy (Chobanian et al., 2003; NHBPEP,
2000).
Beta-adrenergic blocking agents, especially atenolol,
may be associated with fetal growth restriction (Butters,
Kennedy, & Rubin, 1990) and are not preferred in pregnancy unless methyldopa and hydralazine fail to control
blood pressure (Lindheimer & Akbari, 2000). Data on
alpha-adrenergic blockers are anecdotal, and these drugs
are not recommended except in the rare case of pheochromocytoma (Lindheimer & Akbari, 2000).
Calcium channel blockers have had limited use in pregnancy. Concerns have been raised about their effect on
uteroplacental blood flow, but no increase in teratogenicity was noted in one study (Magee et al., 1996). In another study, however, no benefits to the therapy were noted
(Gruppo di Studio Ipertensione in Gravidanza, 1998). In
addition, as stated earlier, they are not approved by the
Food and Drug Administration for treating hypertensive
crises of pregnancy.
Diuretics should not be used as a prophylactic for
preeclamptic hypertension and are not considered the first
line of treatment for chronic hypertension during pregnancy. Diuretics have a role for women whose hypertension occurred prepregnancy or before midpregnancy
(NHBPEP, 2000). However, furosemide should be avoided because it is embryotoxic. Thiazide diuretics have the
safest record for treatment in pregnancy (Collins et al.,
1985).
Antihypertensive Therapy During Lactation
There has been little research on the effects of antihypertensive medications during lactation. Although animal
studies suggest that these drugs are excreted through
breastmilk and short-term studies have not found adverse
effects from methyldopa or hydralazine, no long-term
human studies have discussed the drug effects on infants
(Flack et al., 2002). The reader is referred to the recommendations from the Committee on Drugs of the American Academy of Pediatrics for more information regarding drugs that may be safely used during lactation.
Volume 33, Number 2
Clinical Implications
Assessment
Preventing hypertension-induced problems in pregnancy requires nurses to use their assessment, advocacy, and
counseling skills. Assessment begins with the accuracy of
blood pressure measurements. Checking blood pressures
in pregnant women should never be treated as a routine,
mundane task. Instead, accurate measurement of BP must
be given a high priority, paying careful attention to ensure
the appropriate steps are followed. Because blood pressure drops with the normal cardiovascular changes of
pregnancy, nurses must be aware that BP usually considered “within normal limits” may actually signify impending problems. Systolic blood pressure ≥ 125 mm Hg or ≥
75 mm Hg DBP in mid-pregnancy or ≥ 130 mm Hg SBP
or ≥ 85 mm Hg DBP in later pregnancy indicates problems and should be reported to the physician or midwife
immediately. Women who have a rise of more than 30
mm Hg systolic, or 15 mm Hg diastolic, regardless of the
absolute value, should be monitored closely and their
blood pressure reported. For hospitalized patients, assessing nocturnal blood pressure is important because women
with preeclampsia often experience their highest values at
night.
Nurses also need to assess for subjective complaints
that may indicate serious problems. Visual changes or
severe headaches may be precursors of convulsions in
women experiencing severe preeclampsia. Complaints of
unusual bleeding or bruising are signs of severe
preeclampsia.
If these symptoms occur in combination with epigastric
pain, the patient may be exhibiting signs of the HELLP
syndrome and immediate medical care must be obtained.
Nurses also must report abnormal laboratory studies as
soon as they are detected (see Table 3). Knowing which
tests must be reported immediately requires that nurses
understand the underlying pathology of hypertensive disorders of pregnancy and how that pathology is demonstrated in laboratory studies. In addition to monitoring
maternal health, nurses must also conduct careful fetal
N
urses with strong assessment, counseling,
and advocacy skills can contribute significantly
to the early identification and treatment of
hypertensive problems of pregnancy and to
improved maternal and fetal outcomes.
March/April 2004
assessments, including fetal heart tones and fetal activity,
so that any signs of fetal distress are identified as quickly
as possible.
Patient Advocacy
Nurses also have an important role as patient advocate. It is not sufficient only to alert the physician or midwife of alarming signs and symptoms. The nurse must
also be knowledgeable of NHBPEP-recommended strategies for treating high blood pressure in pregnancy. Awareness of these strategies allows the nurse to advocate for
appropriate care for patients and to challenge care that is
not evidence-based. Such awareness ensures that nurses
do not administer drugs deemed to be inappropriate for
the diagnosis.
Counseling
Counseling is another important skill that must be
employed by any nurse working with pregnant women.
Women need to be instructed about the signs and symptoms they need to report that indicate a problem is developing in the pregnancy. For women who develop
preeclampsia, counseling is required not only in relation
to the disease process and its treatment but also in relation to the emotional toll exacted by the diagnosis. Fears
related to their personal health as well as the possibility of
a fetal death must be addressed. Nurses working in outpatient settings have the opportunity to counsel hypertensive women before conception regarding medication and
lifestyle choices to minimize the risks associated with
chronic hypertension in pregnancy.
Home care nurses may be increasingly called upon to
monitor women with mild preeclampsia in the home setting. They may also provide postpartum care and as such
need to be knowledgeable about postpartum complications of preeclampsia. They may be asked to monitor for
resolution of gestational hypertension and assist women
with chronic hypertension to regain blood pressure control. In addition, nurses in all outpatient settings need to
be aware of the effect of medications on infant development so that appropriate counseling can be given to
women who want to breastfeed their infants.
Conclusion
Hypertensive disorders are a serious problem complicating 6% to 8% of all pregnancies (NHBPEP, 2000).
There are consequences of significant maternal and fetal
morbidity and mortality associated with these disorders.
Nurses are often the frontline health care providers working with at-risk women. Nurses with strong assessment,
counseling, and advocacy skills can contribute significantly to the early identification and treatment of hyper-
JOGNN 217
tensive problems of pregnancy, and therefore, to
improved maternal and fetal outcomes.
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JOGNN 219
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Rosalind M. Peters, PhD, RN, is an assistant professor, College
of Nursing, Wayne State University, Detroit, MI.
John M. Flack, MD, MPH, is a professor and director, Cardiovascular Epidemiology, Department of Internal Medicine,
Wayne State University, Detroit, MI.
Address for correspondence: Rosalind M. Peters, PhD, RN, College of Nursing, Wayne State University, 5557 Cass Ave., Room
358 Cohn Bldg., Detroit, MI 48202. E-mail: rpeters@
wayne.edu.
JOGNN Reviewer Panel: 2004
Vicki Akin, CNS, MSN
Erin Anderson, RN, MSN
Joan Rosen Bloch, PhD, CRNP
Caroline Brown, DEd, CNS, WHNP, IBCLC
Anita Catlin, DNSc, FNP
Sandra K. Cesario, RNC, PhD
Andrea Christian, MS, RN, CNS
Patricia Creehan, RN, MSN, CS
Diane Holditch-Davis, RN, PhD
Barbara Leary Dion, RNC, ICCE, MA, MSN
Pamela Dee Hill, RN, CBE, PhD, FAAN
Debra Hobbins, MSN, APRN, NP
Debra Jackson, RNC, MPH, DSc
Lori Jackson, RNC, NNP
Sheryd J. Jackson, RNC, MS, WHNP
Teresa Johnson, PhD, RN
Susan Kardong-Edgren, RNC, MS, FACCE
Virginia L. Kinnick, RN, CNM, EdD
Gail Schoen Lemaire, PhD, APRN, BC
Lynne P. Lewallen, RN, PhD
Louise K. Martell, RN, MN, PhD
Patricia R. McCartney, RNC, PhD
Kristen Montgomery, RN, PhD
220 JOGNN
Anne A. Moore, RNC, MSN
Dianne Morrison-Beedy, RNC, WHNP, PhD
Mary R. Nichols, RN, CS, FNP, PhD
Susan A. Orshan, RNC, PhD
Cynthia Persily, RN, PhD
Kathie Records, PhD, RN
Michelle Renaud, PhD, RN
Cyndi Roller, WHNP, CNM, PhD
Patsy Ruchala, RN, DNSc
Rebecca B. Saunders, RNC, PhD
Jan Sherman, RN, NNP, PhD
Martha Sleutel, RN, PhD, CNS
Linda Snell, WHNP, DNS
Mary Ann Stark, RNC, MS
Lynn Stover, RN, DSN
Marilyn Stringer, PhD, CRNP, RDM
Rosemary Theroux, RNC, MS, PhD
Lorraine Tulman, DNSc, RN, FAAN
Leona VandeVusse, CNM, PhD, FACNM
Victoria von Sadovsky, PhD, RN
Candy Wilson, RNC, MSN
Jeanne Wilton, RNC, MS, IBCLC, WHNP
Margaret R. Wood, RN, PhD
Volume 33, Number 2