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  • 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


  • Classification of Blood Pressure for Adults Normal SBP 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


  • 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


  • 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


  • 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


  • 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

  • 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 avail