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Hypertensive
disorders in
pregnancy
Lectures 4
Hypertension in Pregnancy
Significance and incidence
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Hypertensive disorders of pregnancy are the
most common medical complication reported
during pregnancy
Preeclampsia complicates approximately 5%
to 10% of all pregnancies
Significant contributor to maternal and
perinatal morbidity and mortality In woman
with history of chronic hypertension or renal
disease predating pregnancy the occurrence
of preeclampsia is 25%
2 2
Hypertension in Pregnancy
Significance and incidence


Preeclampsia predisposes the woman to
potentially lethal complications, including
eclampsia, abruptio placentae, disseminal
intravascular coagulation, acute renal failure,
adult respiratory distress syndrome, cerebral
hemorrhage
Causes of perinatal death related to
preeclampsia are uteroplacental insufficiency
and abruptio placentae, which lead to
intrauterine fetal death, preterm birth, and low
birth weight
3 3
Hypertension in Pregnancy
Significance and incidence



Eclampsia (characterized by seizures) from
profound cerebral effects of preeclampsia is the
major maternal hazard.
As a rule, maternal and perinatal morbidity and
mortality rates are highest among cases in which
eclampsia is seen early in gestation (before 28
weeks), maternal age is greater than 25 years,
the woman is a multigravida, and chronic hypertension or renal disease is present
The fetus of the eclamptic woman is at increased
risk from abruptio placentae, preterm birth,
intrauterine growth restriction (IUGR), and acute
hypoxia
4 4
Hypertension in Pregnancy
Classification
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Chronic hypertension
Pregnancy-induced hypertension
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Gestational hypertension
Preeclampsia
Eclampsia
Preeclampsia superimposed on chronic
hypertension
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Standard definitions are not consistently used by
health care providers
5 5
Chronic hypertension
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
Present before the pregnancy or diagnosed
before week 20 of gestation
or continuing beyond 42 days postpartum
6 6
Gestational hypertension

Onset of hypertension without proteinuria
after the 20th week of pregnancy
Systolic BP > 140 mm Hg
 Diastolic BP >90 mm Hg
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Diagnosis of onset during pregnancy based
on two measurements that meet criteria for
gestational BP elevation within a 1-week
period
7 7
Preeclampsia
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Pregnancy-specific syndrome
Hypertension develops after 20 weeks of gestation in
previously normotensive woman
Proteinuria may be present
Multisystem, vasospastic disease process
characterized by hemoconcentration, hypertension,
and proteinuria
Disease of reduced organ perfusion with presence of
hypertension and proteinuria
Complicates 3% to 7% of all pregnancies
8 8
Proteinuria
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is a concentration of 0.1 g/L (1+ to 2+ on
dipstick measurement) or more in at least
two random urine specimens collected at
least 6 hours apart.
In a 24-hour specimen, proteinuria is a
concentration of 0.3 g/L per 24 hours
9 9
Edema

Pathologic edema is clinically evident,
generalized accumulation of fluid of the
face, hands, or abdomen that is not
responsive to 12 hours of bed rest. It may
also be manifested as a rapid weight gain
of more than 2 kg in 1 week. The
presence of edema is no longer
considered necessary for the diagnosis of
preeclampsia
10 10
Preeclampsia
MILD PREECLAMPSIA
SEVERE PREECLAMPSIA
MATERNAL EFFECTS
Blood pressure
BP reading of 140/90 mm Hg x2, 4-6 hr apart
Rise to >160/110 mm Hg on two separate
occasions 4-6 hr apart with pregnant woman
on bed rest
Mean arterial pressure
(MAP)
>105 mm Hg
>105 mm Hg
Weight gain
Weight gain of more than 0.5 kg/wk during
the second and third trimesters or sudden
weight gain of 2 kg/wk at any time
Same as mild preeclampsia
Proteinuria
— Qualitative dipstick
— Ouantitative 24 hr
analysis
Proteinuria of 0.3 g/L in a 24 hr specimen or
>0.1 g/L in a random day-time specimen on
two or more occasions 6 hr apart (because
protein loss is variable); with dipstick, values
varying from 1+ to 2 +
Proteinuria of >0.5 g/L in 24 hr or >4+
protein on dipstick
Edema
Dependent edema, some puffiness of eyes,
face, fingers; pulmonary edema absent
Generalized edema, noticeable puffiness;
eyes, face, fingers; pulmonary edema
possibly present
Reflexes
May be normal
Hyperreflexia ≥3+, possible ankle clonus11
11
Preeclampsia
MILD PREECLAMPSIA
SEVERE PREECLAMPSIA
MATERNAL EFFECTS
Reflexes
May be normal
Hyperreflexia ≥3+, possible ankle clonus
Urine output
Output matching intake, ≥30 ml/hr or <650
ml/24 hr
<20 ml/hr or <400 ml to 500 ml/24 hr
Headache
Absent/transient
Severe
Visual problems
Absent
Blurred, photophobia, blind spots on
funduscopy
Irritability/changes in
affect
Transient
Severe
Epigastric pain
Absent
Present
Serum creatinine
Normal
Elevated
Thrombocytopenia
Absent
Present
AST elevation
Normal or minimal
Marked
12 12
Preeclampsia
MILD PREECLAMPSIA
SEVERE PREECLAMPSIA
FETAL EFFECTS
Placental perfusion
Reduced
Decreased perfusion expressing as IUGR
in fetus; FHR: late decelerations
Premature placental
aging
Not apparent
At birth placenta appearing smaller than
normal for duration of pregnancy,
premature aging apparent with numerous
areas of broken syncytia, ischemic
necroses (white infarcts) numerous,
intervillous fibrin deposition (red
infarcts)
13 13
HELLP syndrome

is a laboratory diagnosis for a variant of
severe preeclampsia characterized by
hemolysis (H), elevated liver enzymes
(EL), and low platelets (LP)
14 14
Eclampsia
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Seizure activity or coma in woman
diagnosed with preeclampsia
No history of previous seizure disorder
Presentation varies
One third in labor
 One third during delivery
 One third within 72 hours postpartum
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15 15
Chronic hypertension with
superimposed preeclampsia
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Women with chronic hypertension may
acquire preeclampsia or eclampsia
Increases morbidity for mother and fetus
16 16
Etiology
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Unique to human pregnancies
Signs and symptoms develop only during
pregnancy and disappear after birth of the fetus
and passage of placenta
The cause is unknown
Associated high risk factors
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Primigravidity
Multifetal pregnancy
Preexisting medical condition (Obesity, Chronic renal
disease, Chronic hypertension, Diabetes)
Preeclampsia in a prior pregnancy or Family history of
PIH
Maternal age <19 years; >40 years
17 17
Rh incompatibility
18 18
Etiology
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Current theories
Increase vasoconstrictor tone
Abnormal prostaglandin action
Endotelian cell activation
Immunologic factor
Genetic disposition
diet
19 19
Pathophysiology
May be caused by disruptions in placental
perfusion and endothelial cell dysfunction
Main pathogenic factor is not an increase in BP, but
poor perfusion resulting from vasospasm
 Arteriolar vasospasm diminishes diameter of blood
vessels, which impedes blood flow to all organs
and increases BP
 Significant decreases in placental, kidney, liver, and
brain function

20 20
Pathophysiology
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reflects alterations in the normal adaptations of pregnancy.
Normal physiologic adaptations to pregnancy include
increased blood plasma volume, vasodilatation, decreased
systemic vascular resistance, elevated cardiac output, and
decreased colloid osmotic pressure
Pathologic changes in the endothelial cells of the glomeruli
(glomeruloendotheliosis) are uniquely characteristic of
preeclampsia, particularly in nulliparous women (85%).
The main pathogenic factor is not an increase in blood
pressure but poor perfusion as a result of vasospasm.
Arteriolar vasospasm diminishes the diameter of blood
vessels, which impedes blood flow to all organs and raises
blood pressure
Function in organs such as the placenta, kidneys, liver, and
brain is depressed by as much as 40% to 60%
21 21
22 22
HELLP syndrome

Laboratory diagnostic variant (not clinical)
variant of severe preeclampsia involves
hepatic dysfunction, characterized by:
Hemolysis (H)
 Elevated liver enzymes (EL)
 Low platelets (LP)
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23 23
HELLP syndrome
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The exact mechanism is unknown
Arteriolar vasospasm, endothelial damage,
and platelet aggregation with resultant
tissue hypoxia are the underlying
mechanisms for the pathophysiology of
HELLP syndrome
24 24
HELLP syndrome
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epigastric or right upper quadrant
abdominal pain (possibly related to
hepatic ischemia) 65%
nausea and vomiting 50%
25 25
HELLP syndrome
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Lab test
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platelet count less than 100,000/mm3
Elevate liver enzymes levels
aspartate aminotransferase [AST]
alanine aminotransferase [ALT])
evidence of intravascular hemolysis (burr cells on peripheral
smear or elevated bilirubin level)
A unique form of coagulopathy (not DIC) occurs
with HELLP syndrome. The platelet count is low,
but coagulation factor assays,
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prothrombin time
partial thromboplastin time
bleeding time remain normal
26 26
HELLP syndrome

Associated with increased risk for:
Pulmonary edema
 Acute renal failure
 Disseminated intravascular coagulation (DIC)
 Placental abruption
 Liver hemorrhage or failure
 Adult respiratory distress syndrome
 Sepsis
 Stroke
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High risk for maternal death
27 27
Care management
Chronic Hypertension

Chronic hypertension associated with
increased incidence of:
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Abruptio placentae
Superimposed preeclampsia
Increased perinatal mortality
Fetal effects
Fetal growth restriction
 Small for gestational age
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29 29
Chronic Hypertension – cont’d
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Ideally management begins before
conception
Lifestyle changes may be necessary
In postpartum, high risk women
monitored closely for complications
May safely breastfeed even though low
levels of antihypertensive medications will
be in breast milk
30 30
Assessment and nursing diagnosis
Interview
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Medical history
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DM, renal disease, chronic hypertension
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Family history
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Social history (marital, nutritional status, cultural beliefs,
activity level, health habits)
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BP
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Abnormal weight gain
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Increase sign of edema
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Presents of proteinuria
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Headache
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Visual disturbance
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Epigastric pain
31 31
Assessment and nursing diagnosis
Physical examination
 BP
 Observation of edema (distribution, degree, pitting)
 Symptom reflecting central nervous system and visual
system
 Deep tendon reflexes
 Fetal status
 Uterine tonicity
 Sign of progression of mild preeclampsia to severe
preeclampsia or eclampsia
 Respiration (crackles, diminished breath sound)
32 32
33 33
34 34
Assessment and nursing diagnosis
Lab tests
 Complete blood cell count (including a platelet count),
hematocrit, hemoglobin
 Clotting studies (including bleeding time, PT
(protrombine time), PTT (partial thromboplastin time),
and fibrinogen)
 Liver enzymes (lactate dehydrogenase [LDH], AST,
ALT), glucose level
 Chemistry panel (blood urea nitrogen [BUN], creatinine,
glucose, uric acid),
 Type and screen, possible crossmatch
 Proteinuria
35 35
Lab tests
NORMAL
PIH
HELLP
Hemoglobin/hematocrit
12 to 16 gm/dl/37% to
47%
May ↑
↓
Platelets
150,000 to 400,000/mm3
Unchanged
<100,000/mm3
PT/PTT
12 to 14 sec/60 to 70 sec
Unchanged
Unchanged
Fibrinogen
150 to 400 mg/dl
300 to 600 mg/dl
Present
Fibrin split products (FSP)
Absent
Absent
↓
Blood urea nitrogen (BUN)
10 to 20 mg/dl
<10 mg/dl
↑
Creatinine
0.5 to 1.1 mg/dl
<1 mg/dl
↑
Lactate dehydrogenase (LDH)
45 to 90 U/L
Unchanged
↑
Aspartate aminotransferase (AST)
4 to 20 U/L
Unchanged
↑
Alanine aminotransferase (ALT)
3 to 21 U/L
Unchanged
↑
Creatinine clearance
80 to 125 ml/min
130 to 180 ml/min
↓
Burr cells/schistocytes
Absent
Absent
Present
Uric acid
2 to 6.6 mg/dl
4.5 to 6 mg/dl
>10 mg/dl
Bilirubin (total)
0.1 to 1 mg/dl
Unchanged or ↑
↑
36 36
Preeclampsia
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Nursing actions are derived from medical
management, health care provider directives,
and nursing diagnoses.
Early prenatal care, identification of pregnant
women at risk for preeclampsia, and
recognition and reporting of physical warning
signs are essential components in the
optimization of maternal and perinatal
outcomes.
The role of the nurse's skills in assessing the
woman for factors and symptoms of
preeclampsia cannot be overestimated
37 37
Mild preeclampsia

Goal is to ensure maternal safety and
deliver a healthy newborn
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May be safely managed at home by nurse
(2-3 times per week) or by themself
Maternal assessment (weight, urine dipstick
protein determination, BP, DFMC)
 Fetal assessment (ultrasound every 3 weeks,
DFMC, NST or BPP 1-2 times per week
 Activity restriction
 Diet
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38 38
Severe preeclampsia and HELLPsyndrome
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At greater risk for pregnancy complications
Should be hospitalized for at least 24 hours for
observation and treatment if necessary
Intrapartum care
 Magnesium sulfate
 Control of blood pressure
 Postpartum care
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39 39
Severe preeclampsia and
HELLP-syndrome
Antepartum care
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focuses on stabilization and preparation for birth.
Assessments include review of the cardiovascular system,
pulmonary system, renal system, hematologic system, and
CNS.
Fetal assessments for well-being (e.g., NST, BPP, Doppler
velocimetry) are important because of the potential for
hypoxia related to uteroplacental insufficiency.
Baseline laboratory assessments include metabolic studies for
liver enzyme (AST, ALT, LDH) determination, complete blood
count with platelets, coagulation profile to assess for DIC,
and electrolyte studies to establish renal functioning.
Weight is measured on admission and every day thereafter.
40 40
Severe preeclampsia and
HELLP-syndrome
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An indwelling urinary catheter facilitates monitoring of renal
function and effectiveness of therapy.
If appropriate, vaginal examination may be done to check for
cervical changes.
Abdominal palpation establishes uterine tonicity and fetal
size, activity, and position.
Electronic monitoring to determine fetal status is initiated at
least once a day.
The woman's room must be close to staff and emergency
drugs, supplies, and equipment. Noise and external stimuli
must be minimized. Seizure precautions are taken
Bed rest is commonly ordered.
41 41
Severe preeclampsia and
HELLP-syndrome

Intrapartum nursing care
involves continuous monitoring of maternal
and fetal status as labor progresses. The
assessment and prevention of tissue hypoxia
and hemorrhage, both of which can lead to
permanent compromise of vital organs,
continue throughout the intrapartum and
postpartum periods (Leicht & Harvey, 1999).
42 42
Severe preeclampsia and
HELLP-syndrome
Magnesium sulfate
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As prophylaxis against convulsion
I/V as a secondary infusion to the main intravenous (IV) line
by volumetric infusion pump
An initial loading dose of 4 to 6 g of MgSO4 per protocol or
physician's order is infused over 20 to 30 minutes. This dose
is followed by a maintenance dose of magnesium sulfate
that is diluted in an IV solution per physician's order (e.g.,
40 g of magnesium sulfate in 1000 ml of lactated Ringer's
solution) and administered by infusion pump at 1 to 3 g/hr.
This dose should maintain a therapeutic serum Mg level of 4
to 8 g/dl.
Serum magnesium levels are obtained after the patient has
received magnesium sulfate for 4 to 6 hours.
43 43
Severe preeclampsia and HELLPsyndrome Magnesium sulfate
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Intramuscular (IM) MgSO4 is seldom used because
absorption rate cannot be controlled, injections are
painful, and tissue necrosis may occur.
However, the IM route may be used with some women
who are being transported to a tertiary care center.
The IM dose is 4 to 5 g given in each buttock, a total of
10 g (with 1% procaine possibly being added to the
solution to reduce injection pain), and can be repeated
at 4-hour intervals.
Z-track technique should be used for the deep IM
injection, followed by gentle massage at the site.
44 44
Severe preeclampsia and HELLPsyndrome Magnesium sulfate
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Magnesium sulfate interferes with the release of acetylcholine at the
synapses,
decreasing neuromuscular irritability,
depressing cardiac conduction,
and decreasing CNS (central nervous system) irritability.
Because magnesium circulates free and unbound to protein and is
excreted in the urine, accurate recordings of maternal urine output must
be obtained.
Diuresis is an excellent prognostic sign; however, if renal function
declines, all of the magnesium sulfate will not be excreted and can cause
magnesium toxicity.
Serum magnesium levels are obtained on the basis of the woman's
response and if any signs of toxicity are present.
Early symptoms of toxicity include nausea, a feeling of warmth, flushing,
muscle weakness, decreased reflexes, and slurred speech.
45 45
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Severe preeclampsia and
HELLP-syndrome
Magnesium
sulfate
Deep tendon reflexes
Urine output
Respiration rate
Consciousness
If magnesium toxicity is suspected, the infusion should be
discontinued immediately.
Calcium gluconate, the antidote for magnesium sulfate, may also be
ordered (10 ml of a 10% solution, or 1 g) and given by slow IV push
(usually by the physician) over at least 3 minutes to avoid undesirable
reactions such as arrhythmias, bradycardia, and ventricular fibrillation.
Because magnesium sulfate is also a tocolytic agent, its use may
increase the duration of labor. A preeclamptic woman receiving
magnesium sulfate may need augmentation with oxytocin during
labor. The amount of oxytocin needed to stimulate labor may be more
than that needed for a woman who is not on magnesium sulfate.
46 46
Severe preeclampsia and
HELLP-syndrome
antihypertensive agent
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Starts if diastolic pressure is higher than 100 to 110 mm Hg
Order to decrease the diastolic blood pressure to 90 to 100
mm Hg
Prevent left ventricular failure and cerebral hemorrhage.
decrease the arterial pressure too much or too rapidly
agent of choice is
hydralazine IV
labetalol hydrochloride IV
methyldopa orally
Nifedipine orally
47 47
Eclampsia

Premonitory signs and symptoms
Headache
 Blurred vision
 Severe epigastric pain
 Altered mental status

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Tonic- clonic convulsions
Hypotension
Coma
48 48
Eclampsia

Immediate care
Ensure a patent airway
 Patient safety a major concern
 Post-seizure decision regarding timing and
method of birth

49 49
Eclampsia
TONIC-CLONIC CONVULSION SIGNS
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Stage of invasion: 2 to 3 sec, eyes are
fixed, twitching of facial muscles occurs
Stage of contraction: 15 to 20 sec, eyes
protrude and are bloodshot, all body
muscles are in tonic contraction
Stage of convulsion: muscles relax and
contract alternately (clonic), respirations
are halted and then begin again with long,
deep, stertorous inhalation, coma ensues
50 50
EclampsiaINTERVENTION

Keep airway patent: turn head to one
side, place pillow under one shoulder or
back if possible Call for assistance Protect
with side rails up Observe and record
convulsion activity
51 51
Eclampsia AFTER CONVULSION
OR SEIZURE
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Do not leave unattended until fully alert
Observe for postconvulsion coma, incontinence
Use suction as needed
Administer oxygen via face mask at 10 L/min
Start IV fluids and monitor for potential fluid overload
Give magnesium sulfate or other anticonvulsant drug as ordered
Insert indwelling urinary catheter
Monitor blood pressure
Monitor fetal and uterine status
Expedite laboratory work as ordered to monitor kidney function, liver
function, coagulation system, and drug levels
Provide hygiene and a quiet environment
Support and keep woman and family informed
Be prepared for delivery when woman is in stable condition
52 52
Postpartum nursing care
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After birth the symptoms of preeclampsia or eclampsia resolve quickly,
usually within 48 hours.
The hematopoietic and hepatic complications of HELLP syndrome may
persist longer.
These patients often show an abrupt decrease in platelet count, with a
concomitant increase in LDH and AST levels, after a trend toward
normalization of values has begun. Generally the laboratory
abnormalities seen with HELLP syndrome resolve in 72 to 96 hours.
Blood pressure is measured at least every 4 hours for 48 hours or
more frequently as the woman's condition warrants.
Even if no convulsions occurred before the birth, they may occur
within this period.
MgSO4 infusion may be continued 12 to 24 hours after the birth.
Assessments for effects and side effects continue until the medication
is discontinued.
53 53
Postpartum nursing care
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The woman is at risk for a boggy uterus and a large lochial flow as a result of
the magnesium sulfate therapy. Uterine tone and lochial flow must be
monitored closely.
The preeclamptic woman is unable to tolerate excessive postpartum blood loss
because of hemoconcentration. Oxytocin or prostaglandin products are used
to control bleeding.
Ergot products (e.g., Ergotrate, Methergine) are contraindicated because they
can increase blood pressure.
The woman is asked to report symptoms such as headaches and blurred
vision.
The nurse assesses affect, level of consciousness, blood pressure, pulse, and
respiratory status before an analgesic is given for headache.
Magnesium sulfate potentiates the action of narcotics, CNS depressants, and
calcium-channel blockers; these drugs must be administered with caution.
The woman may need to continue an antihypertensive medication regimen if
her diastolic blood pressure exceeds 100 mm Hg at discharge.
54 54