Hypertension in Pregnancy

Education Consultants SSM Healthcare – 2014

Objectives

1. Describe the classification of hypertensive disorders of pregnancy.

2. Describe the pathophysiology of preeclampsia. 3. Discuss patient assessment for preeclampsia. 4. Summarize the management of mild and

severe preeclampsia. 5. Describe the use of magnesium sulfate for

seizure prophylaxis. 6. 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 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

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

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%

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 renin-aldosterone 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: Altered proangiogenic and antiangiogenic

factor balance Increase maternal oxidative stress Endothelial dysfunction Immunologic dysfunction

Pathophysiology of Preeclampsia: The Maternal Syndrome

vasospasm – vasoconstriction ↑BP

disruption of endothelial lining of blood vessels

plasma and colloids escape

platelets activated to repair damage

movement of fluid from intravascular to interstitial space

edema, hemoconcentration

poor perfusion, including placenta

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 … 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

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) 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 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 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 1.7-2.1 mg/dl Therapeutic range 4.8 – 9.6 (5-8) Loss of DTRs 8-12 Feelings of warmth, flushing 9-12 Somnolence 10-12 Slurred speech 10-12 Muscular paralysis 15-17 Respiratory difficulty 15-17 Cardiac arrest 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) 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)

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 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. 863-912). New York: Churchill Livingstone.

Simpson, K.R., & Creehan, P.A. (Eds.). (2014). AWHONNs, perinatal nursing (4th ed.). Philadelphia: Lippincott.