Subject: Obstetrics

Topic: 3.06 Hypertension in Pregnancy

Lecturer: Dr. Nagtalon
Date: October 1, 2015

OUTLINE NIHHP Working Group Definition

I. Introduction
II. Classification of Hypertensive disorders
III. Causes of HPN in Pregnancy
IV.
V.
Etiopathogenisis
Preeclampsia
VI. Prevention of Preeclampsia
VII. Seizure prevention
VIII. Expectant vs. Labor Induction
IX. Eclampsia
X. HELLP Syndrome
XI. Chronic Hypertension
Reminder: Please take note that the ACOG guidelines for Hypertension in Pregnancy was
used as a reference for this lecture. You can access the guidelines through the link
attached at the end of this trans. Happy studying!
I. INTRODUCTION
 “It is a concern in Obstetrics because of the association with the
need for preterm delivery. Especially if patient develop severe
disease at anytime of pregnancy. If we need to weigh the benefits
and risks in favor of either the mother & the baby, there is usually
a need to terminate or deliver a preterm baby and with
prematuity, there a lot of physical and neurocognitive
dysfunction.”
 Advanced maternal age, ART-related pregnancies, multifetal
gestation, genetic predisposition in some, and lifestyle largely
contribute to the increasing incidence of pregnancies complicated
with HPN.
BURDEN
 Global data shows that the incidence of HPN in pregnancy is 12-
22%; mortality at 17.6 %
 “Incidence has been increasing primarily because women now get
pregnant at a later age. Before, target age is having a child
between ages 23 – 27. Because of a change in lifestyle & focus on
professionalism, mothers elect to embark on pregnancy at a later
age ”
 POGS Statistics: maternal deaths due to HPN 26.24% (2010)
 Incidence in USA has reached 25%.
 Every year close to 500,000 women die from complications
related to pregnancy
 Nearly 10% of maternal deaths in Asia and Africa, and 25% in
Latin America are associated with hypertensive disorders of
pregnancy.
 Major contributor to prematurity and maternal morbidity and
mortality.
 Considering the multi-systemic nature of preeclampsia, it is now a
risk factor for later-life CVD and metabolic disease in women.
 Curbing maternal Mortality &Morbidity from hypertensive
disorders in pregnancy will result not only in less lives lost, but
also in less deprivation of resources.
 For each of these deaths, there are 50-100 other women who
experience “near miss” significant morbidity that stops short of
death but results in health risk and health care cost.
 The majority of deaths related to hypertensive disorders can be
avoided by providing timely and effective care to women
presenting with such complications.
 “If she has the risk factors for developing hypertension during
pregnancy, there has to be close evaluation. Physician should look
for symptoms that will make her consider the possibility of this
woman eventually developing HPN in pregnancy. And these are:
Sudden increase in weight not related to nutrition, Edema and
headache or epigastric pain. This can be subtle signs of
hypertension & progressive disease”
Hypertension in Pregnancy:
 BP=/>140/90 (on 2 separate readings) or,
 Diastolic BP ≥ 110 mmHg (single reading)
This reading should be confirmed over several hours in a day. In
clinical practice, the definition varies, however, the NIHHP adopted
this definition.
Renal Function
 Proteinuria: excretion of 300mg in 24-hr urine or a 24-hr urine
protein/creatinine ratio of at least 0.3 mg/dl
 Hypertension with proteinuria: Preeclampsia
 Hypertension without proteinuria: Gestational Hypertension
 >20 weeks AOG: Gestational Hypertension
 <20 weeks AOG: Chronic Hypertension
II. CLASSIFICATION OF HYPERTENSIVE DISORDERS OF PREGNANCY
1. Preeclampsia –Eclampsia
2. Chronic HPN
3. Chronic HPN with superimposed preeclampsia
4. Gestational Hypertension
PREECLAMPSIA & ECLAMPSIA
 Because of the syndromic nature of preeclampsia, the
dependence of the diagnosis on proteinuria has been eliminated.
 In the absence of proteinuria, the diagnosis is made in association
with:
o thrombocytopenia (platelet count < 100,000/microliter)
o impaired liver enzymes (elevated blood levels of liver
transaminases to twice the normal concentration)
o new development of renal
o pulmonary edema
o new-onset cerebral or visual disturbances.
CHRONIC HYPERTENSION
 High BP known to predate conception or detected before 20
weeks of gestation
CHRONIC HYPERTENSION WITH SUPERIMPOSED PREECLAMPSIA
 chronic HPN in association with preeclampsia
 Diagnosis is more likely in the following 7 scenarios: women with
hypertension only in early gestation who develop proteinuria
after 20 weeks of gestation and women with proteinuria before
20 weeks of gestation who:
1) Experience a sudden exacerbation of hypertension, or a
need to escalate the antihypertensive drug dose especially
when previously well controlled with these medications;
2) Suddenly manifest other signs and symptoms, such as an
increase in liver enzymes to abnormal levels;
3) Present with a decrement in their platelet levels to below
100,000/microliter;
4) Manifest symptoms such as right upper quadrant pain and
severe headaches;
5) Develop pulmonary congestion or edema;
6) Develop renal insufficiency
7) Have sudden, substantial, and sustained increases in
protein excretion

Trans Group: Ev, Nikki, Ava, Alex Page 1 of 7

Edited By: Mabie Minor
 If the only manifestation is elevation in BP to levels < 160 mm Hg
systolic and 110 mm Hg diastolic and proteinuria, this is
considered to be superimposed preeclampsia without severe
features. The presence of organ dysfunction is considered to be
superimposed preeclampsia with severe features.

GESTATIONAL HYPERTENSION
 BP elevation after 20weeks gestation in the absence of
proteinuria or the systemic findings in preeclampsia.
 Failure of BP to normalize postpartum is a chronic hypertension.

III. CAUSES OF HYPERTENSION IN PREGNANCY

Figure 2. Placental Angiogenesis in Preeclampsia
 Strong genetic predisposition (4-8 fold increase)
-A woman w/ an affected mother has a 4-fold increased
 In preeclampsia, there may be incomplete trophoblastic invasion.
chance of having the condition compared to the general
The myometrial vessels do not lose their endothelial and
population; 8-fold increased risk w/ an affected sister.
musculoelastic tissue, and their mean external diameter is only
 40% increase in the rate of pre-eclampsia since 1990, as a result half that of vessels in normal placentation.
of a rise in advanced maternal age and ART-related multiple
 Thus, it is likely that the abnormally narrow spiral arteriolar
births
lumen impairs placental blood flow. Diminished perfusion with
 Primipaternity hypoxia lead to release of placental debris inciting systemic
 Thrombophilia – because of inherent abnormality in inflammatory response.
hematopoietic system
Immunologic Theory
IV. ETIOPATHOGENESIS
 The cascade of events leading to the preeclamptic syndrome is a
result of a host of abnormalities that result in vascular and
endothelial damage and subsequent vasospasm, transudation of
plasma and ischemic and thrombotic sequelae.

NORMAL PLACENTAL ANGIOGENESIS

Figure 3. Immunologic Theory

“Th1 is a bad cytokine, associated with inflammatory changes. So, if

you have a lot of this because of reduced immunosuppressive HLA-G,
you can have an alter prostacyclin thromboxane ratio then if you have
alteration, you have more vasoconstriction that lead to microvascular
coagulation & capillary permeability”

Faulty Placental Angiogenesis

Figure 1. Prostacyclin-dependent low resistance uteroplacental unit
 Uterine spiral arterioles undergo extensive remodelling, to allow
a 4-fold rise in U-P blood flow, as they are invaded by
endovascular trophoblasts.
 Ingrowth of trophoblastic cells into tunica media of spiral
arterioles replace the vascular endothelial and muscular linings
and result to denervation & loss of muscular & elastic
components allowing these vessels dilatation & elongation to a
“cork-screw/saw-tooth” configuration. It should be able to stand
the increase in blood flow from the maternal to fetal system.
 Such changes extend to the decidual & myometrial portions, &
are fully established by 20wks AOG.
 Although the cause remains unknown, evidence for its
manifestation begins early in pregnancy with covert
pathophysiological changes that gain momentum across
gestation and eventually becomes clinically apparent.
 Unless delivery supervenes, these changes ultimately results to
multi-organ damage with a clinical spectrum ranging from barely
noticeable to one cataclysmic pathophysiological deterioration
that can be life-threatening to both mother and fetus.

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Figure 4. Faulty Placental Angiogenesis.
Basic pathology: Endothelial dysfunction (Remember!)
CASE I
 At 30weeks AOG a previously normotensive 36y/o primigravida
(conception post ovulation induction with IUI), with a family
history of HPN, presents with the following:
Weight gain: 10 lbs in 4 weeks (normal: 1 lb per week)
BP=140/90
Random urine protein (++) (proteinuria)
1) Is this a case of hypertension in pregnancy, or are the findings
usually expected during the third trimester?
Answer: This is hypertension in pregnancy. It is not chronic
hypertension because it manifested at 30 weeks and she was
previously normotensive. It might be preeclampsia but further
confirmatory tests are needed.
2) What should be done?
Less than 37weeks AOG:
 In-patient or out-patient management but the patient has
to be counselled that she has to monitor her blood pressure
at least twice in one sitting per week.
 Maternal evaluation twice weekly.
 Baseline of liver function (transaminases), renal function
(creatinine ) and CBC (haemoglobin, platelet)
 Fetal evaluation: twice weekly NST, growth assessment
 Ultrasound – check for interval fetal growth and status and
if there is anything that would suggest growth failure then
proceed to Doppler velocimetry.
 If the patient’s blood pressure is 140/90 and not 160/110,
there is still room for expectant management. No need to
deliver because delivering a preterm baby can be very
devastating.
V. PREECLAMPSIA
 Pregnancy-specific hypertensive disease with multisystem
involvement.
 Occurs after 20 weeks of gestation, most often near term, and
can be superimposed on another hypertensive disorder.
 Occurrence of new-onset hypertension plus new-onset
proteinuria (Remember! Excretion of 300mg in 24-h urine)
MANAGEMENT OF PREECLAMPSIA
 The close monitoring of women with gestational HPN or
preeclampsia without severe features, with serial assessment of
maternal symptoms and fetal movements, serial BP (2x weekly)
and assessment of platelet and liver enzymes (weekly) is
suggested. (QOE: Moderate; SOR: Qualified)
o There is no need to give anti-hypertensive medications if
blood pressure is less than 160/110 because it will just
compromise the circulation of the fetus which will make
them small for gestational age or growth restricted. Severe
IUGR can lead to intrauterine death.
 In those with preeclampsia without severe features,
ultrasonography use to assess fetal growth and antenatal testing
(NST) to assess fetal status is suggested. (QOE: Moderate ;SOR:
Qualified)
 Should there be evidence of fetal growth restriction in affected
women, umbilical artery Doppler velocimetry as adjunct
antenatal test is recommended. (QOE: Moderate; SOR: Strong)
MANAGEMENT OF PREECLAMPSIA <37 WEEKS AOG
 Elect prompt delivery in the presence of:
o Labor or ROM
o Abnormal / deteriorating maternal-fetal status
(hemoconcencration, increase in liver enzymes and increase
in creatinine)
o EFW <5th percentile or abnormal doppler flow
o Suspected abruption (This might be due to constriction of
blood vessels. Upon physical examination, the uterus is
tender and fetal heartbeat is absent on Doppler.)
 Watch out for severe headache, visual changes, epigastric pain
and shortness of breath.
Mild Gestational HPN or Preeclampsia at or beyond 37weeks AOG
 Delivery is recommended
 Manner of Delivery: vaginal route preferred provided there is no
absolute indication for a cesarean section
 37 weeks is term and signifies good outcome for the baby
TIMING OF DELIVERY: Risk Benefit Ratio
 Expectant management is associated with development of:
o severe HPN: 10-15%
o eclampsia: 0.2-0.5%
o HELLP syndrome: 1-2%
(Hemolysis, Elevated Liver enzymes and Low Platelet)
o fetal growth restriction: 10-12%
o Abruption placenta: 0.5-2%
o IUFD: 0.2-0.5%
 Immediate delivery is associated with increased NICU admission
due to respiratory complications, slight increase in neonatal death
in those born <37weeks AOG
 In the case, the patient’s status and the fetal status, BP and fetal
growth were assessed with the following results:
o Baseline maternal and fetal status were reassuring.
o No increase in BP was noted.
o Fetal growth was according to the expected for the AOG.
 So she was advised to continue maternal and fetal status
monitoring twice weekly and to seek immediate consult for any of
the following (signs of impending eclampsia):
o headache
o visual disturbance
o epigastric pain
o difficulty of breathing
 From recording: The decision is still in favor of what is going to be
good for both the mother and baby. Counseling should be very
thorough so that the family can make an informed decision.
Immediate delivery might be associated with increased NICU stay.
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 In the presence of severe disease (eclampsia), then it would be
easy to make the decision to terminate the pregnancy. Otherwise
be more conservative rather than aggressive.
Once the pregnancy reaches 37 weeks, there is a need to deliver
even if hypertension is mild because if you extend further this may
cause IUFD. It is not always cesarean delivery. There is still a
chance to have vaginal birth. Bishop score is also applied in
patients with hypertension beyond 37 weeks.
CASE II
 At 36weeks AOG, she complained of severe headache and later
on developed seizures and thus rushed to the ER.
Initial assessment:
o post-ictal
o BP=150-160/100
o If fetal heart is bradycardic and irregular, the baby should
be delivered.
 Hydralazine was started for BP=160/110.Hypertensives should be
given because the BP is already 160/110.
 MgSO4 drip was added to the regimen. Because it decreases
recurrence of seizures in patients with severe pre-eclampsia. It is
given at 4-6 grams loading dose IV and maintained at 2 grams per
hour for at least 24 hours. The patient must be monitored for
several parameters because it can cause central depression. She
should be check on her mentation, respiratory rate, reflexes and
urine output. The favourable level is between 4-7 meq.
1) Diagnosis? Eclampsia because of presence of seizures
2) Is there room for expectant management? Regardless of
age of pregnancy, once eclampsia sets in, the baby has to
be delivered but the mother has to be stabilized first. If it is
less than 34 weeks AOG, there is still a chance to stimulate
fetal lung maturity by giving antenatal corticosterioids
(betamethasone at 12 mg IM given in 2 doses 24 hours
apart). The mother can also be given MgSO4 in order to
prevent recurrence of seizures.
 Blood was extracted for CBC with platelet count, blood typing,
LDH, SGOT, creatinine.
Results showed:
o Low haemoglobin
o Platelet 90,000 / mm3 (lower limit: 100,000)
o LDH and SGOT twice normal
o Creatinine 2mg/dl (increased).
1) What do the test results suggest? This suggests HELLP syndrome
which may lead to DIC.
2) Should delivery be delayed until after the liver and renal
function return to normal baseline? There is no room for
conservative management. Prompt delivery should be instituted
usually through cesarean section
3) Should delivery be decided, how and what type of anesthesia
should be considered? If platelet count is decreasing, any
regional anesthesia can incite bleeding and this patient may
have intraspinal bleed. The lower limit is at least 80,000 mm3.
This patient can still have epidural anesthesia.
 Recommendation: For preeclampsia with severe features, at or
beyond 34 weeks AOG, and in those with unstable maternal /
fetal condition regardless of age, delivery is recommended. (QOE:
Moderate; SOR: Strong)
 Remember: For mild hypertension and pre-eclampsia without
severe features, expectant management can be done. At 37
weeks, delivery should be done regardless of condition. If less
than 34 weeks with severe features (eclampsia and/or HELLP
syndrome), prompt delivery should be made.
 A cesarean section under epidural anesthesia was performed
with delivery of a healthy male, 2500gms (normal), APGAR 9,9.
Estimated blood loss = 1000ml (normal)
1) Propose a postpartum plan for this patient.
She had severe hypertension, eclampsia and HELLP syndrome so
close monitoring should be instituted (liver, renal and
hematopoietic functions) and anti-hypertensives should be
started.
2) What are the issues in regard breastfeeding?
There is no contraindication to breastfeeding unless she is taking
ACE-inhibitors. The antihypertensives given are usually
hydralazine and nifedipine (category B drugs).
3) What are the options for conception control?
She can take anti-contraceptives only if the blood pressure has
gone back close to normal and there are no contraindications
like migraine because this can increase her risk for
thromboembolism.
4) Can recurrence of the condition be prevented?
Recurrence rate is high (25% if pre-eclampsia and 75% if
gestational hypertension). This can be prevented by giving her
calcium 2 grams per day if dietary history is low calcium and low
dose aspirin.
VI. PREVENTION OF PREECLAMPSIA
 Calcium supplementation for populations of low calcium intake
 LDA for those at high risk
 Goal of anti-HPN therapy in progressive disease: prevent
complications
o Maternal:
 CVA- leading cause of maternal mortality due to loss of
cerebral autoregulatory mechanisms, resulting in
increased CBF, rising CPP & vessel rupture
 Cardiac failure
 Liver rupture
 Eclampsia
 HELLP
 Pulmonary Edema
 Preterm delivery
o Fetal:
 Hypoxia
 IUGR
 Prematurity, IUFD, Anemia secondary to abruptio placenta
 (From Williams, not discussed by lecturer) Various strategies are
used to prevent or modify preeclampsia severity have been
evaluated. However, none of these has been found to be
convincingly and reproducibly effective
o Dietary manipulation: low salt diet, calcium or fish oil
supplementation
o Exercise: physical activity, stretching
o Cardiovascular Drugs: diuretics, antihypertensive drugs
o Antioxidants: ascorbic acid (Vit C), alpha tocopherol (Vit E),
Vitamin D
o Antithrombotic drugs: low dose aspirin,
aspirin/dipyridamole, aspirin+heparin, aspirin +ketanserin
CONTROLLING BP ( 160/100 mmHg)
 CVA can be prevented by BP control.
 If target BP is not achieved despite maximum dose an additional
or alternative drug must be utilized.
 HPN crises usually occurs at BP >240/140 mmHg, for which
SODIUM NITROPRUSSIDE is necessary and should be managed by
someone skilled at critical care
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  MgSO4
o 4-6 g IV over 15-30 mins., then 2 g/hrinfusion for 24 hrs
(therapeutic 4-7 meq/l)
o Adverse Effects: Respiratory depression (12meq/L), Loss of
patellar reflexes (10meq/L) , and Central Depression
o 10% Calcium gluconate1gm IV to reverse AE
o Who should be given MgS04?
 In a woman with new onset proteinuric HPN at atleast
one of the following is required:
 BP 160/110 mmHg
 Proteinuria +2 or more
 Serum Creatinine >1.2 mg/dL
 Platelet count <100,000 µL
 Aspartate transaminase (AST) elevated 2x above
Figure 5. Drugs for controlling BP
upper limit of normal
 Persistent headache, scotoma
PERSISTENT UNCONTROLLED HYPERTENSION  Persistent mid-epigastric, RUQ pain
 If a patient develops a true hypertensive crisis with hypertensive
encephalopathy (generally occurs at BP 240/140 mmHg) then SEIZURE PREVENTION IN SEVERE PREECLAMPSIA
emergent intervention with a rapidly acting agent such as sodium
 MgSO4 for seizure prophylaxis (Level Ia, A)
nitroprusside is necessary and should be management by someone
 RR of eclampsia 0.33(95% CI 0.11-1.02)
skilled in critical care and the use of such drugs.
 MgSO4 superior than phenytoin
 Sodium Nitroprusside
o Rapidly acting agent effective in many cases
o Dose: 0.25-8 µg/kg/minute as IV infusion, start with 0.3- 0.5
µg/kg/min (about 20-50 µg/min), then 1- 3 µg/kg/min IV
(max:<10 µg/kg/min) (50 mg in 250 ml D5W)
o Onset: 0.5-1 min; Duration: 2-5 hours
o Decreased efficacy in those with renal failure
 Labetalol
o Mixed alpha/beta blocker, excellent for most hypertensive
emergencies
o Dose: 20-80mg IV bolus every 10 minutes or 0.5-2mg/min
infusion IV
Start 20 mg IV, then 20- 80 mg q10 min prn, or start with 0.5
mg/min infusion, then 1- 2 mg/min (may be up to 4 mg/min)
IV infusion up to 300 mg/d max.
o Onset: 5 -10 min; Duration: 3- 6 h
o Not for those w/ heart block, bradycardia, CHF, asthma,
severe bronchospasm

VII. SEIZURE PREVENTION

Figure 7. Schematic clinical management algorithm for suspected severe

preeclampsia at <34 weeks (William’s)

Figure 6. Seizure Prevention (WHO 2011).

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 VIII. EXPECTANT vs. LABOR INDUCTION
 The optimal management is delivery in severe-pre-eclampsia,
eclampsia
Figure 8. Optimal Management (WHO 2011)
A. GLUCOCORTICOID THERAPY
 If there are concerns about prematurity, treatment decreased
incidence of RDS and improved fetal survival (Leveno and
Cunningham 2009)
 Evidence very low for corticosteroid use to ameliorate HELLP
syndrome (WHO 2011 and Katz and colleagues 2008)
IX. ECLAMPSIA
 Eclampsia is defined by ACOG as the convulsive phase of
preeclampsia and can be considered a more severe
manifestation of the disease.
 It is a convulsion in a woman with preeclampsia that cannot be
attributed to another cause (William’s)
 Seizures are generalized and may appear before, during, or after
labor (William’s)
 It is often preceded by premonitory events such as severe
headaches and hyperreflexia and may also occur in the absence
of warning signs.
MANAGEMENT OF ECLAMPSIA
 Does not always require emergency CS
 Goals to achieve before delivery:
o Interventions for BP control
o Seizure control with MgSO4
o Prevention of recurrence
 Delivery is an option after conditions have been stabilized
 Method of delivery depends on gestational age, fetal
presentation, and the status of the cervix
 Interventions may include cardiotocography assisted 2nd stage
labor and use of oxytocin during the 3rd stage
 Avoid prolonged labor
X. HELLP SYNDROME
COMPONENTS
 Hemolysis (≥ 2 of the following):
o Peripheral smear containing schistocytes and burr cells
o Serum bilirubin at 1.2 mg/dL
o Severe anemia unrelated to blood loss
 Elevated liver enzymes
o AST or ALT 2x upper limit of normal
o LDH 2x upper limit of normal
 Low platelet count ( < 100,000/cu mm)
MANAGEMENT OF HELLP SYNDROME
 Continue MgSO4 until there is laboratory evidence of
improvement in platelet count and transaminases
 Proceed with delivery when condition has stabilized or if there is
presence of fetal compromise
 Use of dexamethasone in this situation remains controversial
XI. CHRONIC HYPERTENSION
 Obesity and advanced maternal age at childbirth equated with
the rise in prevalence of chronic hypertension
 It has a 4.6 – 22.3% incidence among women aged 30 – 39 years
and 0.6 – 2% among those in the 18 – 29 age group
DEFINITION
 BP ≥ 140/90 mm Hg before pregnancy or before 20 weeks AOG
or both
 Chronic hypertension is associated with fetal growth restriction
resulting in SGA infants (30%) and preterm deliveries (60%)
 Perinatal mortality is increased when chronic hypertension is
superimposed with preeclampsia
 Chronic HPN also has the highest risk for abruption placenta
o 1.5% risk among those with mild HPN
o 5 – 10% in severe HPN
o 30% with superimposed preeclampsia
CHRONIC HPN WITH SUPERIMPOSED PREECLAMPSIA
 Some women with chronic HPN develop abnormally high blood
pressure which typically occurs after 24 weeks
 If new-onset or worsening baseline HPN is accompanied by new-
onset proteinuria or other findings listed in the table below, a
diagnosis of chronic HPN with superimposed preeclampsia is
confirmed
Figure 9. Criteria for Chronic HPN with Superimposed Preeclampsia
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  Risk factors for preeclampsia include:
o Previous preeclampsia (32% risk)
o Duration of hypertension (>4 years  32% risk)
o Diastolic BP > 110 mm Hg (40-50%)
o Proteinuria (27%)
o Thrombophilia (40-50%)
o DM (30-40%)

MANAGEMENT OF CHRONIC HYPERTENSION

Diagnosis
 Early prenatal care for women with chronic HPN includes early
diagnosis
 Hypertensive disorders can create difficult problems with
diagnosis and management in women who are not first seen
until after midpregnancy
o This is due to the physiologic decrease in blood pressure
during the second and early third trimester among both
normotensive and chronic hypertensive women
o Thus, women with previously undiagnosed chronic vascular
diseases who are seen before 20 weeks frequently present
with normal BPs.

Prenatal Care
 Preconception education and counseling
 Regular prenatal visits
 Evaluation for end-organ disease
 Anti-HPN medications with few fetal side-effects
o Methyldopa
- actively transported to CSF & brain
- inhibits neurotransmission of norepinephrine within
medullary centers which control BP
- outflow of sympathetic nerve impulses to the CVS is
reduced  decreased BP
o Labetalol
- Hypotensive effect from vasodilatation induced by
blockade of α1 adrenoceptors and activation of β2
adrenoceptors on vascular smooth muscles
- Blockade of β2 adrenoceptors in the heart  minimizes
reflex increase in CO  hypotensive effect
 Fetal surveillance for growth, umbilical artery via Doppler
Studies
 Close monitoring for superimposed preeclampsia

REFERENCES
 ACOG Guidelines on Hypertension in Pregnancy
http://www.acog.org/Resources-And-Publications/Task-Force-
and-Work-Group-Reports/Hypertension-in-Pregnancy
 Lecture ppt
 Recording
 William’s

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