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Hypertension in
Pregnancy
Education Consultants
SSM Healthcare – 2014
Objectives
1. Describe the classification of hypertensive
2.
3.
4.
5.
6.
disorders of pregnancy.
Describe the pathophysiology of preeclampsia.
Discuss patient assessment for preeclampsia.
Summarize the management of mild and
severe preeclampsia.
Describe the use of magnesium sulfate for
seizure prophylaxis.
Review the management of eclamptic seizures.
Hypertensive Disorders
of Pregnancy . . .
Complicate 10% of all pregnancies
Accounted for 15.7% of maternal
mortality in the U.S. from 1991-1999
Current Terminology
and Classification of
Hypertension in Pregnancy
 National High Blood Pressure Education Program Working Group
on High Blood Pressure in Pregnancy (2000)
 ACOG Practice Bulletin Number 33: Diagnosis and Management
of Preeclampsia and Eclampsia (2002)
 Joint National Committee on Prevention, Detection, Evaluation,
and Treatment of High Blood Pressure (2004)
 ACOG Task Force on Hypertension in
Pregnancy (2013) Hypertension in
Pregnancy
Hypertension is Defined as . . .
 Systolic blood pressure ≥ 140 mmHg or
 Diastolic blood pressure ≥ 90 mmHg
 Based on at least two measurements taken
4-6 hour apart (or 2 separate visits)
 Accurate and consistent BP assessment is
important
Classification of
Blood Pressure for Adults
 Normal – SBP <120 and DBP <80
 Prehypertension – 120–139 or 80–89
 Hypertension Stage 1 – 140–159 or 90–99
 Hypertension Stage 2 – >160 or >100
 Joint National Committee on Prevention, Detection, Evaluation,
and Treatment of High Blood Pressure (2004)
Classification of Hypertensive
Disorders in Pregnancy
 Gestational hypertension
 Preeclampsia-Eclampsia
 Chronic hypertension
 Chronic hypertension with superimposed
preeclampsia
Gestational Hypertension
 New onset blood pressure elevation after 20
weeks of gestation in the absence of
proteinuria or other systemic findings indicative
of preeclampsia
 Incidence
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Nulliparous women 6%-18%
Multiparous women 6%-8%
Markedly increased in twin gestations
Higher rates of induction of labor and cesarean
birth
Preeclampsia/Eclampsia
 Preeclampsia is a pregnancy specific
hypertensive disease with multisystem
involvement
 Usually occurs after 20 weeks gestation
 Incidence

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
Nulliparous women 3%-7%
Multiparous women 0.8%-5%
Markedly increased in twin gestations
 Eclampsia is the convulsive phase of the
disorder
Preeclampsia/Eclampsia
Risk Factors for Preeclampsia
 Primiparity
 Previous preeclamptic pregnancy
 Chronic HTN or chronic renal disease or both
 History of thrombophilia
 Mutifetal pregnancy
 In vitro fertilization
 Family history of preeclampsia
 Type I or Type II diabetes mellitus
 Obesity
 Systemic lupus erythematosus
 Advanced maternal age (older than 40 years)
Chronic Hypertension
 Hypertension that predates pregnancy
 Or, is detected before 20 weeks of gestation
Chronic Hypertension with
Superimposed Preeclampsia
 Chronic hypertension in association with
preeclampsia
 Prognosis much worse than for either condition
alone
Maternal Mortality Rate from
Preeclampsia or Eclampsia
 1.8 per 100,000
 The incidence of preeclampsia has increased by 25%
in the U.S. in the past two decades
 Hypertension is directly responsible for 17.6% of
maternal deaths in the U.S. (ACOG, 2002)
 Large racial disparity, African-American women are
more likely to die of preeclampsia than are women of
all other races
 Outcome is usually dependent on gestational age at
the onset and the severity of the disease process
Maternal Complications
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Placental abruption
Thrombocytopenia
Disseminated intravascular coagulation (DIC)
Cerebral hemorrhage
Hepatic failure
Subcapsular hematoma of the liver → rupture
Acute renal failure
Pulmonary edema
ARDS
Cesarean birth
Fetal/Neonatal Complications
 Placental insufficiency
Intrauterine growth restriction
 Hypoxia
 Intrauterine fetal demise

 Acute insult with placental abruption
 Acute insult with maternal seizure
 Preterm birth
 Oligohydramnios
Normal Physiology of Pregnancy
 50% increase in blood volume
 35-50% increase in cardiac output
 Increased uterine blood flow

From 50 mL to 600 mL per minute
Uncomplicated Pregnancies Become
a Markedly Vasodilated State
 Peripheral resistance decreases by 25%
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Vessels develop resistance to the pressor effects
of angiotensin II
Increased prostaglandin synthesis with an
increase in the potent vasodilator prostacyclin
Increased nitric oxide synthase
Increased production of the endothelium-derived
relaxing factor
Changes Also Occur in the
Renal System
 Renal blood flow and
glomerular filtration rate
increase, activating the reninaldosterone system and
resulting in a falling BP
Resulting in …
 BP decreasing in the first 2 trimesters
 BP usually falling 10 mm Hg by mid-pregnancy,
then slowly approaching pre-pregnancy levels in
the 3rd trimester
Etiology of Preeclampsia
 Preeclampsia is a multisystemic disease that
affects all organ systems and is far more than
high blood pressure and renal dysfunction.
 Despite considerable research, the etiology of
preeclampsia remains unclear.
The Prevailing Theory
 The placenta is evident as the root cause of
preeclampsia.
 It is proposed that an immunologically
initiated reduction in trophoblast invasion
leads to failed vascular remodeling of the
maternal spiral arteries that perfuse the
placenta.
 Altered placental function (placental hypoxia
and ischemia) leads to the maternal disease.
Pathophysiology of
Preeclampsia Occurs
in Two Stages
1. Alterations in Placental Perfusion
2. Maternal Syndrome
The Link Between the Two
Stages
 Includes a cascade of secondary effector
mechanisms including:
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Altered proangiogenic and antiangiogenic
factor balance
Increase maternal oxidative stress
Endothelial dysfunction
Immunologic dysfunction
Pathophysiology of Preeclampsia:
The Maternal Syndrome
vasospasm – vasoconstriction
↑BP
poor perfusion, including placenta
edema, hemoconcentration
movement of fluid from
intravascular to interstitial
space
disruption of endothelial
lining of blood vessels
platelets activated to
repair damage
plasma and colloids escape
Effects of Vasospasm and
Vasoconstriction
normal RBCs & platelets
platelets agglutinate, fibrin forms
Hemolysis – damage or destruction
of RBCs – schistocytes & burr cells
Vessel Damage
leakage of plasma & colloids
into interstitial space
Renal Involvement
 Glomerular endothelial damage & fibrin
deposition leads to ischemia
 ↓ Renal blood flow and
 ↓ glomerular filtration rate
 Proteinuria
 ↓ Uric acid clearance,
↑ serum uric acid
 ↓ Creatinine clearance,
↑ serum creatinine
 Oliguria
Acute renal failure
Liver Involvement
 Hepatic dysfunction is part of HELLP syndrome
 Late hepatic changes are consistent with hepatic
infarction and hepatocellular necrosis
 Signs of liver failure: malaise, nausea, epigastric
pain, hypoglycemia, hemolysis, anemia
 Hepatic changes can lead
to subcapsular hematoma
which can result in liver rupture
CNS Involvement
 Vasoconstriction results
in widespread
microvascular cerebral
changes and ischemia
 Cerebral edema
 Hyperreflexia
 Headache
 Nausea & vomiting
 CVA
 May induce seizures –
the eclamptic phase
Other Organ System Involvement
 Pulmonary
 Pulmonary edema – endothelial injury leading to fluid
leakage and potential volume overload
 Ophthalmic Involvement
 Retinal arteriolar spasms – scotoma, photophobia,
blurring, or double vision
 Coagulation Involvement
 Coagulation Involvement
 Endothelial damage consumes
platelets
Symptoms of Preeclampsia
 Swelling of the face or hands
 Headache that will not go away
 Visual disturbances
 Pain in upper right quadrant
 Nausea or vomiting
 Sudden weight gain
 Difficulty breathing
Severe Preeclampsia
Management of Preeclampsia
 Delivery is the only cure
 Deliver when most optimal for mother and fetus
 Little data to suggest any therapy alters the
underlying pathophysiology
 Interventions designed to safeguard mother
while allowing time for fetal maturity
Management of Preeclampsia
 Careful monitoring
 Hospitalization frequently advised
 Ongoing assessment: symptoms, VS, DTRs,
fetal well-being (NST, BPP, Growth evaluation)
 Control of BP
 Antihypertensive therapy warranted for
BP ≥160/110 or rapidly rising
 In pregnant adolescent, may use at DBP 100
 Prevention of eclamptic seizures
 Timely delivery
Management of Mild Gestational
HTN or Preeclampsia
Management of Severe
Preeclampsia at <34 Weeks
Systematic Nursing
Assessment is Essential
 Cardiovascular
 CNS
 Renal
 GI/Hepatic
 Fetal well-being
 Psychosocial
Hospital Safety Measures
 Low lighting
 Quiet environment (limit phone, TV, visitors)
 Airway, O2, suction at bedside
 Emergency medications available
In the Event of Eclampsia …
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Prevent maternal injury
Lateral positioning
Maintain airway – do not insert a tongue blade
Suction
Oxygen
Give adequate magnesium sulfate
Fetal assessment and labor assessment
Seizure and blood pressure control first then
plan for delivery
HELLP Syndrome
 A laboratory, not a clinical diagnosis
 Appears in 2%-12% of preeclamptic women
 Hemolysis
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Peripheral smear with burr cells
Elevated bilirubin level
 Elevated Liver Enzymes

Elevated AST and ALT
 Low Platelets

>100,000/mm3
HELLP Syndrome
 More common in older, Caucasian, multiparous
women
 About 90% of women report a history of
malaise for several days
 About 65% of women have epigastric or right
upper quadrant abdominal pain
 About 50% of women develop nausea and
vomiting
Fetal Assessment
 Fetal activity, kick counts
 FHR pattern, continuous monitoring
 FHR variability
 Review NST and BPP
 Review growth curves per
ultrasound. IUGR often precedes
preeclampsia.
 Notify nursery & pediatrician
 Potential for neonatal
hypermagnesemia
Medications
 Magnesium sulfate
 Antihypertensives – avoid ↓ BP < 140/90
 Steroids for fetal lung maturity or for HELLP
syndrome
 Diuretics – only in pulmonary edema
 Avoid sedatives and valium
Magnesium Sulfate
 Elevated magnesium levels depress the CNS
 Also acts as a cerebral vasodilator to counteract
the cerebral hypoxia and increases blood flow to
the brain
 Affects the neuromuscular and neurocellular
signal transmission, which inhibits seizure
activity
 Also decreases levels of the neurotransmitter,
acetylcholine
Magnesium Sulfate
 4-6 g loading dose IV over 15-30 minutes
 1-3 g continuous IV
 Always give IVPB with a pump
 Monitor for side effects and toxicity
 Cautious use of narcotics or CNS depressants
 Antidote: Calcium gluconate


Available at bedside
10 ml of 10% solution (equal to 1 g) slow IV
push over 3-10 minutes
Magnesium Sulfate on the FBP
 Bolus of 2 grams in 50 mL
 Bolus of 4 grams in 100 mL
 Bolus of 6 grams in 150 mL
 For any bolus . . . Set the rate at 300 mL/hr
(this equates to 1 gm/5 minutes)
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2 grams in 50 mL will infuse in 10 minutes
4 grams in 100 mL will infuse in 20 minutes
6 grams in 150 mL will infuse in 30 minutes
 Nurse remains at the bedside . . .

VS every 15 minutes with oxygen saturation
monitoring
Magnesium Sulfate on the FBP
 Maintenance 20 grams in 500 mL
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1 gram/hr
25 mL/hr
2 grams /hr 50 mL/hr
3 grams/hr 75 mL/hr
 Reminder card for your ID badge . . .
Side Effects
 Flushing
 Sweating
 Lower maternal temperature
 Nausea and Vomiting
 Headache
 Blurred vision
 Shortness of breath, chest pain, &
pulmonary edema
Side Effects/Signs of Toxicity
 Respiratory depression (respirations < 12/min)
 Shortness of breath, chest pain, abnormal
breath sounds, cough pulmonary edema
 Hypotension
 Bradyarrhythmias
 Muscle weakness
 Diminished/absent DTRs
 CNS depression – somnolence, marked
lethargy
Magnesium Sulfate
 Nursing Care
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Monitor for toxicity
Assess VS (respiratory rate), DTRs, and urine
output before and during administration
Continuous fetal assessment
 Institute for Safe Medication Practices –
List of High-Alert Medications
 High-alert medications are drugs that bear a
heightened risk of causing significant patient
harm when they are used in error.
Magnesium Sulfate
 Half-life with normal renal function = 4 hours
 90% excreted in 24 hours
 Signs of moderate toxicity include respiratory
depression and arrhythmia
 If respiratory alterations occur, turn off before
notifying physician
 Possible alternative – Phenytoin (Dilantin)
Magnesium Toxicity
Normal
Therapeutic range
Loss of DTRs
Feelings of warmth, flushing
Somnolence
Slurred speech
Muscular paralysis
Respiratory difficulty
Cardiac arrest
1.7-2.1 mg/dl
4.8 – 9.6 (5-8)
8-12
9-12
10-12
10-12
15-17
15-17
20-35
Sibai, B.M. (2002).
Deep Tendon Reflexes
 Imperative nursing function with Magnesium
Sulfate administration
 Determine need for magnesium therapy
 Evaluate efficacy of magnesium therapy
 Prevent toxicity from magnesium therapy
DTRs function as a window into the CNS.
Tips on Taps (Checking DTRs)
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Assess biceps and patellar reflexes and ankle clonus
Ensure relaxation of the limb
Feel the tendon (if you can’t feel it, don’t tap)
Tap lightly
Reinforce the reflex, rather than tapping harder
Assess upper and lower extremities in the same session
Interpret the results 0 to 4
Assigning plus or minus notations creates problems
Biceps DTR
 Elbow at a 90° angle
 Arm slightly bent
down
 Grasp the elbow
 Press thumb against
the biceps brachii
tendon
 Strike your thumb –
vary your thumb
pressure with each
blow
Patellar Reflex
 Put your hand under the knee (thigh) and lift it
from the bed. Tap the patellar tendon directly.
Responding to DTRs
 Hyperreflexia (3 or 4)

A sign the disease has affected the cortex, the
pt needs magnesium started or increased
 Normoreflexia (2)

Proper dosing achieved
 Hyporeflexia or areflexia (1 or 0)
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Decrease or discontinue infusion, with physician
order
If respiratory depression, turn off infusion even
before calling physician
Nursing Actions to Promote Safety
 All loading doses, dosage changes and new
infusion bags started must have pump settings
checked by two registered nurses – document
in EPIC
 Purple tape is placed around each bag, on the
tubing by the attachment to the pump, and on
the tubing by the attachment to the mainline
 When the magnesium infusion is discontinued
the bag should be disconnected from the
mainline
Antihypertensives in Preeclampsia
 Hydralazine (Apresoline) - Vasodilator
 Labetalol hydrochloride – Beta-blocker
 Methyldopa (Aldomet) – Maintenance therapy
 Nifedipine (Procardia) – Calcium-channel
blocker – relaxes arterial smooth muscle – use
with caution if patient is also getting
magnesium sulfate due to possible potentiation
of CNS effects
For Urgent BP Control in
Pregnancy
Common Oral Antihypertensive
Agents in Pregnancy
Labetalol hydrochloride
 Hypertension: initial, 100 mg ORALLY twice daily
 Maintenance, 200-400 mg ORALLY twice daily
 Hypertension: IV to ORAL conversion, initial, 200 mg
ORALLY, followed in 6-12 hr by 200-400 mg ORALLY
depending on BP response
 Hypertension (Severe): Repeated IV injection: Initial
dose of 20 mg (0.25 mg/kg) by slow injection over 2
minutes; repeat injections of 40 or 80 mg at 10 minute
intervals as indicated; MAXIMUM dose is 300 mg;
maximum effects occur within 5 minutes of injection
 Hypertension (Severe): May be used as a continuous
infusion of 1mg/kg per hour as needed.
 Watch for a delayed effect of sudden maternal
hypotension. Use with caution in women with asthma.
Hydralazine (Apresoline)
 Essential hypertension – emergency therapy:
20 to 40 mg/dose IM/IV bolus as needed
 Pregnancy: 5 mg IV over 1-2 minutes, may
give another 5-10 mg after 20 minutes
 Maximal effect in 20 minutes
 Recheck BP every 5 minutes
Nifedipine (Procardia)
 Calcium channel blocker
 Uses: Hypertension and angina, off label for
preterm labor
 Dosage: Extended release 30 mg – 60 mg
daily
 Acute hypertension: Short acting 10 mg PO,
repeat every 20-30 minutes to a maximum of
30 mg
 Warnings/Precautions: Can cause
hypotension and fluid retention
Other Issues
 Fluid management – 100-125 mL per hour (?)
 Analgesia and anesthesia
 Method of delivery and timing of delivery
 Potential transfer issues
 Prolonged bedrest
 Psychosocial and emotional support
 Postpartum management
Postpartum Management
 Continue intense assessment and
interventions for 24-48 hours
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Seizure activity and pulmonary edema are
common
In HELLP, increasing platelets indicate
improvement more than BP or output
 Increased potential for uterine atony,
hemorrhage, and volume depletion
 Remember, NSAIDS can contribute to
elevated BP
Postpartum Hypertension
 Preeclampsia can first develop in the
postpartum period
 Thus mandating instruction at discharge
regarding symptoms that should be reported
Final Reminder – Goals of Therapy
1.Ensure maternal safety
2.Deliver a healthy newborn
Nurses do make a
difference!
References
 ACOG. (2013). Hypertension in pregnancy.
 Gilbert, E., & Harmon, J. (2003). High risk
pregnancy and delivery (3rd ed.). St. Louis: Mosby.
 Lowdermilk, D.L., & Perry, S.E. (2004). Maternity
and Women’s Health Care (8th ed.). St. Louis,
Missouri: Mosby.
 Sibai, B.M. (2007). Hypertension. In S.G. Gabbe,
J.R. Niebyl, & J.L. Simpson (Eds.), Obstetrics:
Normal and problem pregnancies (5th ed, pp. 863912). New York: Churchill Livingstone.
 Simpson, K.R., & Creehan, P.A. (Eds.). (2014).
AWHONNs, perinatal nursing (4th ed.). Philadelphia:
Lippincott.