Hyper / Hypo Disorders
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Transcript Hyper / Hypo Disorders
Summer 2013
Risk Factors
Age – under 17 over 35
Gravida and Parity
Socioeconomic status
Psychological well-being
Predisposing chronic illness – diabetes, heart
conditions, renal
Pregnancy related conditions – hyperemesis
gravidarum, gestational hypertension
Goals of Care for High Risk
Pregnancy
© Provide optimum care for the mother and the fetus
© Assist the client and her family to understand and
cope through education
Abortions
Termination of pregnancy at any time before the fetus
has reached the age of viability
Either:
spontaneous – occurring naturally
induced – artificial
Types of Abortions
Threatened
Imminent
Complete
Incomplete
Missed
Recurrent/Habitual
Question???
What are two main complications related to a missed
abortion?
1.
2.
Cerclage procedure -- purse-string
suture placed around the internal os
to hold the cervix in a normal state
Nursing Care post cerclage
Bedrest in a slight trendelenberg position
Teach
Assess for leakage
Assess for contractions
Assess fetal movement and report decrease movement
Assess temperature for elevation
Key Concepts Related to
Bleeding Disorders
If a woman is Rh-, RhoGam is given within 72 hours of
abortion
Provide emotional support. Feelings of shock or
disbelief are normal
Encourage to talk about their feelings. It begins the
grief process
Ectopic Pregnancy
Implantation of the blastocyst in ANY site other
than the endometrial lining of the uterus
ovary
(5) Cervical
Early:
Assessment
Ectopic Pregnancy
• Missed menstruation followed by vaginal bleeding
(scant to profuse)
• Unilateral pelvic pain, sharp abdominal pain
• Referred shoulder pain
• Cul-de-sac mass
Acute:
•
•
•
•
Shock – blood loss poor indicator
Cullen’s sign -- bluish discoloration around umbilicus
Nausea, Vomiting
Faintness
Treatment Options / Nursing Care
Combat shock / stabilize cardiovascular
• Type and cross match
• Administer blood replacement
• IV access and fluids
Laparotomy
Psychological support
Linear salpingostomy
Methotrexate – used prior to rupture. Destroys fast growing
cells
Gestational Trophoblastic Disease
Hydatiform Molar Pregnancy
A DEVELOPMENTAL
ANOMALY OF THE
PLACENTA WITH
DEGENERATION OF THE
CHORIONIC VILLI
As cells degenerate, they
become filled with fluid and
appear as fluid filled grapesize vessicles.
Assessment:
Vaginal Bleeding -- scant to profuse, brownish in color
(prune juice)
Possible anemia due to blood loss
Enlargement of the uterus out of proportion to the
duration of the pregnancy
Vaginal discharge of grape-like vesicles
May display signs of pre-eclampsia early
Hyperemesis gravidarium
No Fetal heart tone or Quickening
Abnormally elevated level of HCG
Question 6
Interventions and Follow-Up
Empty the Uterus by D & C or Hysterotomy
Extensive Follow-Up for One Year
• Assess for the development of choriocarcinoma
• Blood tests for levels of HCG frequently
• Chest X-rays
• Placed on oral contraceptives
• If the levels rise, then chemotherapy started usually
Methotrexate
Critical Thinking Exercise
A woman who just had an evacuation of a hydatiform
mole tells the nurse that she doesn’t believe in birth
control and does not intend to take the oral
contraceptives that were prescribed for her.
How should the nurse respond?
Placenta Previa
Low implantation of the placenta in the uterus
Etiology
• Usually due to reduced vascularity in the upper
uterine segment from an old cesarean scar or fibroid
tumors
Three Major Types:
• Low or Marginal
• Partial
• Complete
Question 8
Interventions and Nursing Care
Placenta Previa
Bed-rest
Assessment of bleeding
Electronic fetal monitoring
If it is low lying, then may allow to deliver vaginally
Cesarean delivery for All other types of previa
Abruptio Placenta
Premature separation of the placenta from the
implantation site in the uterus
Etiology:
ª Chronic Maternal Hypertension
ª Short umbilical cord
ª Trauma
ª History of previous delivery with separation
ª Smoking / Caffeine / Cocaine
ª Vascular problems such as with diabetes
ª Multigravida status
ª Defined as marginal, partial or complete
Treatment and Nursing Care
Abruptio Placenta
Cesarean delivery immediately
Combat shock – blood replacement / fluid replacement
Blood work – assessment for complication of DIC
Placenta Previa
• PAINLESS vaginal bleeding
Abruptio Placenta
Bleeding accompanied by
• Bright red bleeding
• First episode of bleeding is
slight then becomes
profuse
Signs of blood loss
comparable to extent of
bleeding
Uterus soft, non-tender
Fetal parts palpable; FHT’s
countable and uterus is not
hypertonic
Blood clotting defect
absent
•
•
•
•
PAIN
Dark red bleeding
First episode of bleeding
usually profuse
Signs of blood loss out of
proportion to visible amount
Uterus board-like, painful
and low back pain
Fetal parts non-palpable,
FHT’s non-countable and
high uterine resting tone
(noted with IUPC)
Blood clotting defect (DIC)
likely
Signs of Concealed Hemorrhage
Increase in fundal height
Hard, board-like abdomen
High uterine baseline tone on electronic fetal
monitoring
Persistent abdominal pain and low back pain
Systemic signs of hemorrhage
Critical Thinking
Mrs. A., G3 P2, 38 weeks gestation is admitted
to L & D with scant amount of dark red
bleeding. What is the priority nursing
intervention at this time?
A. Assess the fundal height for a decrease
B. Place a hand on the abdomen to assess if hard,
board-like, tetanic
C. Place a clean pad under the patient to assess the
amount of bleeding
D. Prepare for an emergency cesarean delivery
Disseminated Intravascular
Coagulation (DIC)
Anti-coagulation and Pro-coagulation
effects existing at the same time.
Etiology
Defect in the Clotting Cascade
An abnormal overstimulation of the
coagulation process
Activation of Coagulation with
release of thromboplastin into maternal bloodstream
Thrombin (powerful coagulant) is produced
Fibrinogen fibrin which enhances platelet aggregation and clot
formation
Widespread fibrin and platelet deposition in capillaries and
arterioles
Etiology continued
Resulting in Thrombosis (multiple small clots)
Excessive clotting activates the fibrinolytic system
Lysis of the new formed clots create fibrin split
products
These products have anticoagulant properties and
inhibit normal blood clotting
A stable clot cannot be formed at injury sites
Hemorrhage occurs
Ischemia of organs from vascular occlusion of
numerous fibrin thrombi
Multisite hemorrhage results in shock and can result
in death
Assessment & Intervention
Precipitating factors
Abruption
PIH/HELLP syndrome
Sepsis
Anaphylactoid Syndrome
Labs to review
PT, PTT, Platelets, D-Dimer, FSP
Interventions
Remove the cause
Replace fluids (Blood or blood products)
Meds
Assessment/Signs and Symptoms
Spontaneous bleeding – from gums and nose
(epistaxis, injection and IV sites, incisions)
Excessive bleeding – Petechiae and ecchymosis at site
of blood pressure cuff, pulse points
Tachycardia, diaphoresis, restlessness, hypotension
Hematuria, oliguria, occult blood in stool
Altered LOC if cerebral circulation is decreased or
cerebral bleed
Diagnostic Tests
Lab work reveals:
PT – Prothrombin time is prolonged
PTT – Partial thromboplastin time increased
D-Dimer – increased, product that results from fibrin
degradation. More specific marker of the degree of
fibrinolysis
Platelets – decreased, thrombocytopenia
Fibrin Split Product – increased
An increase in both FSP and D-dimer are indicative of
DIC
Assessment
Persistent nausea and vomiting
Weight loss from 5 - 20 pounds
May become severely dehydrated with oliguria
AEB increased specific gravity, and dry skin
Depletion of essential electrolytes
Metabolic alkalosis -- Metabolic acidosis
Starvation
Nursing Care / Interventions
Hyperemesis Gravidarium
Control vomiting
Maintain adequate nutrition and electrolyte balance
Allow patient to eat whatever she wants
If unable to eat – Total Parenteral Nutrition
Combat emotional component – provide emotional
support and outlet for sharing feelings
Mouth care
Weigh daily
Check urine for output, ketones
Classification of HTN in Pregnancy
Gestational HTN = BP > or equal to 140/90 after 20
weeks (replaces term of PIH), protein negative or trace
Pre-eclampsia = BP > or equal to 140/90 after 20 weeks,
proteinuria, edema considered nonspecific
Eclampsia = Progression of pre-eclampsia to
generalized seizures not attributable to other causes
Chronic HTN = BP > or equal to 140/90 that was known
to exist before pregnancy or develops prior to 20 weeks
gestation or does not resolve after 6 weeks after
delivery
Predisposing Factors
Primigravida
Multiple gestation pregnancy
Vascular Disease
Age >35
Obesity
Hydatiform Molar Pregnancy
Family History
Lower SES (poor nutrition,/decreased protein intake,
inadequate prenatal care)
PATHOLOGICAL CHANGES
Gestational Hypertension due to:
GENERALIZED
ARTERIOLAR
CYCLIC
VASOSPASMS
(decrease in diameter
of blood vessel)
INCREASED PERIPHERAL
RESISTANCE;
IMPEDED BLOOD FLOW
(
in blood pressure)
Endothelial
CELL DAMAGE
Intravascular
Fluid Redistribution
Decreased Organ
Perfusion
Multi-system failure Disease
Rationale for HYPERTENSION
The blood pressure rises due to:
ARTERIOLAR VASOSPASMS AND
VASOCONSTRICTION causing
(Narrowing of the blood vessels)
an increase in peripheral resistance
fluid forced out of vessels
HEMOCONCENTRATION
Increased blood viscosity = Increased hematocrit
Key Point to Remember !
HEMOCONCENTRATION develops because:
Vessels became narrowed forcing fluid to shift out of the
vascular space
Fluid leaves the intravascular space
and moves to extravascular spaces
Now the blood viscosity is increased
(Hematocrit is increased)
**Very difficult to circulate thick blood
Proteinuria
With renal vasospasms, narrowing of glomerular
capillaries which leads to decreased renal perfusion
and decreased glomerular filtration rate
PROTEINURIA
Spilling of 1+ of protein is significant to begin treatment
Oliguria and tubular necrosis may precipitate
acute renal failure
Significant Lab Work
Changes in Serum Chemistry
Decreased urine creatinine clearance (80-130 mL/
min)
Increased BUN (12-30 mg/dl.)
Increased serum creatinine (0.5 - 1.5 mg/dl)
Increased serum uric acid (3.5 - 6 mg/dl)
Weight Gain and Edema
Clinical Manifestation:
Edema may appear rapidly
Begins in lower extremities and moves
upward
Pitting edema and facial edema are
late signs
Weight gain is directly related to
accumulation of fluid
The Nurse Must Know
The difference between dependent
edema and generalized edema is
important.
The patient with pre-eclampsia has
generalized edema because fluid is in
all tissues.
Placenta
Due to Vasospasms and Vasoconstriction of the
vessels in the placenta.
Decreased Placental Perfusion and Placental
Aging
Positive CST / __________Decelerations
With Prolonged decreased Placental Perfusion:
Fetal Growth is retarded - IUGR, SGA
Oliguria – 100ml/4 hrs or less than 30 ml. /
hour
Edema moves upward and becomes
generalized (face, periorbital, sacral)
Excessive weight gain – greater than 2 pounds
per week
Central Nervous System Changes
Cerebral edema -- forcing of fluids
to extracellular
Headaches -- severe, continuous
Hyperreflexia
LOC changes – changes in affect
Convulsions / seizures
Visual Changes
Retinal Edema and spasms leads to:
Blurred vision
Double vision
Retinal detachment
Scotoma (areas of absent or depressed
vision)
Nausea and Vomiting
Epigastric pain –often sign of
impending coma
Mild Pre-eclampsia
Systolic> or = to 140/90 but <160 mm
Hg
Diastolic > or = to 90 but < 110 mm Hg
Protein > or = to 0.3 g but < 2 g in 24
hr specimen (1-2+ dipstick)
Creatinine , serum normal
Platelets normal
ALT/AST normal or minimal increase
Urine output normal
No HA
Absent RUQ pain/ no N/V
Absent to minimal visual changes
No pulmonary edema or heart failure
Normal fetal growth
Severe Pre-eclampsia
> or = to 160 mm Hg 2 readings 6 hrs
apart on bedrest
> or = to 110mm Hg
Protein > or = to 5 g in 24 hr specimen
(3+ or higher dipstick)
Creatinine elevated > 1.2 mg/ dL
Platelets decreased < 100, 000 cells/mm3
ALT/AST Elevated levels
Oliguria common, often <500 ml/day
HA Often present
N&V, epigastric pain may be present,
often precedes seizures
Visual disturbances common
May be present
IUGR, reduced amniotic fluid
Interventions and Nursing Care
Home Management
Decrease activities and promote bed rest
Sedative drugs
Lie in left lateral position
Remain quiet and calm – restrict visitors
and phone calls
Dietary modifications
increase protein intake to 70 - 80 g/day
maintain sodium intake
Caffeine avoidance
Weigh daily at the same time
Keep record of fetal movement - kick counts
Check urine for Protein
Hospitalization
If symptoms do not get better then the patient
needs to be hospitalized in order to further
evaluate her condition.
Common lab studies:
CBC, platelets; type and cross match
Renal blood studies -- BUN, creatinine,
uric acid
Liver studies -- AST, ALT, LDH, Bilirubin
DIC profile -- platelets, fibrinogen, FSP,
D-Dimer
Hospital Management
Nursing Care Goal
1. Decrease CNS Irritability
2. Control Blood Pressure
3. Promote Diuresis
4. Monitor Fetal Well-Being
5. Deliver the Infant
Decrease CNS Irritability
Provide for a Quiet Environment and Rest
1. MONITOR EXTERNAL STIMULI
Explain plans and provide Emotional Support
Administer Medications
1. Anticonvulsant -- Magnesium Sulfate
2. Sedative -- Diazepam (Valium)
3. Vasodilator-- Apresoline (hydralazine)
Assess Reflexes
Assess Subjective Symptoms
Keep Emergency Supplies Available
Magnesium Sulfate
ACTION
CNS Depressant, reduces CNS irritability
Calcium channel blocker- inhibits cerebral
neurotransmitter release
ROUTE
IV effect is immediate and lasts 30 min.
IM onset in 1 hour and lasts 3-4 hours
Prior to administration:
Insert a foley catheter with urimeter for
assessment of hourly output
Magnesium Sulfate
NURSING IMPLICATIONS
1. Monitor respirations > 14-16; < 12 is critical
2. Assess for hyporeflexia -- D/C if hyporefexia
3. Measure Urinary Output >100ml in 4 hrs.
4. Measure Magnesium levels – normal is 1.5-2.5 mg/dl per hr
Therapeutic is 4-8mg/dl.; Toxicity - >9mg/dl;
Absence of reflexes is >10 mg/dl;
Respiratory arrest is 12-15 mg/dl;
Cardiac arrest is > 15 mg/dl.
Have Calcium Gluconate available as antagonist
Test Yourself !
A Woman taking Magnesium Sulfate has a
respiratory rate of 10. In addition to discontinuing
the medication, the nurse should:
a. Vigorously stimulate the woman
b. Administer Calcium gluconate
c. Instruct her to take deep breaths
d. Increase her IV fluids
Control Blood Pressure
Check B / P frequently.
Give Antihypertensive Drugs
Hydralazine
Labetalol
Nifedipine
Check Hematocrit
•Do NOT want to decrease the B/P too low or too rapidly. Best
to keep diastolic ~90.
•WHY?
Promote Diuresis
**Don’t give Diuretic, masks the symptoms of
Gestational Hypertension
Bed rest in left or right lateral position
Check hourly output -- foley catheter with
urimeter
Dipstick for Protein
Weigh daily -- same time, same scale
Monitor Fetal Well-Being
FETAL MONITORING-- assessing for late decelerations.
NST -- Non-stress test
CST –contraction stress test
BPP –biophysical profile
If all else fails ---- Deliver the baby!!
HELLP Syndrome
A multisystem condition that is life
threatening and complicates 10% of
pregnancies in women with severe HTN and
may occur during PP period
H = hemolysis of RBC
EL = elevated liver enzymes
LP = low platelets <100,000mm3
(thrombocytopenia)
Etiology of HELLP
Hemolysis occurs from fragmentation and destruction
of erythrocytes leading to anemia
Release of bilirubin R/T liver impairment and
hemolysis of erythrocytes causing
hyperbilirubinemia
Elevated liver enzymes occur from blood flow that is
obstructed in the liver due to fibrin deposits
Vascular vasoconstriction endothelial damage
platelet aggregation at the sites of damage low
platelets
HELLP Syndrome Assessment:
1. Prominent symptom is right upper quadrant pain, lower
chest or epigastric
2. Nausea and vomiting
3. Severe edema
4. Flu like symptoms
5. Avoid traumatizing the liver, restrict palpation of
abdomen
6. This patient needs to be managed in a critical care setting due
to severity of condition
HELLP
Intervention:
1.
Bedrest – any trauma or increase in intraabdominal pressure could lead to rupture
of the liver capsule hematoma.
2. Volume expanders
3. Antithrombic medications
4. Includes all care directed at management of
pre- eclampsia and eclampsia
T O R C H A Infections
T = Toxoplasmosis
O = Other
Syphilis, Gonorrhea,
Chlamydia,Hepatitis A or B
R = Rubella
C = Cytomegalovirus
H = Herpes
A = Aids
Urinary Tract Infection
Most common infection complicating
Pregnancy
Etiology
Pressure on ureters and bladder causing
Stasis with compression of ureters
Reflux
Hormonal effects cause decrease tone of
bladder
Assessment
Dysuria, frequency, urgency
lower abdominal pain; costal vertebral pain
fever
Group B Streptoccocus Infection
(GBS)
Leading cause of life-threatening perinatal infections
Gram positive bacteria colonizes the rectum, vagina,
cervix and urethra of pregnant and non-pregnant
women
Associated with PROM and preterm birth
60% chance of transmission to NB
Fetal effects
Sepsis
Pneumonia
Meningitis
Therapeutic Management
Routine culture for all pregnant women between 35-37
weeks gestation
PCN drug of choice to decrease risk of transmission to
fetus
Risk for transmission to fetus is at time of labor so no
treatment until patient presents in labor
Administer PCN IV every 4 hours until delivery
Toxoplasmosis
Etiology
Protozoan infection. Raw meat and cat litter
Maternal and Fetal Effects
Mom - flu-like symptoms, lymphadenopathy
Fetus – stillborn, premature birth, microcephaly;
mental retardation
* Instruct to cook meat thoroughly
* Avoid changing cat litter
* Advise to wear gloves when working in
the garden
Treatment: Sulfa drugs
Syphilis
Etiology
• Spirochete – Treponema Pallium
Maternal and Fetal Effects
May pass across the placenta to fetus
causing spontaneous abortion. Major cause
of late, second trimester abortion
Infant born with congenital anomalies
Syphilis
Intervention:
• 1. Penicillin
• 2. Advise to return for prenatal visits
monthly to assess for re-infection
• 3. Advise that if treated early, fetus may not
be infected
Gonorrhea
Etiology – Neisseria Gonorrhoeae
Maternal and Fetal Effects:
May get infected during vaginal delivery
causing Ophthalmia neonatorium
(blindness) in the infant
Mom will experience dysuria, frequency,
urgency
Major cause Pelvic Inflammatory Disease
which leads to infertility.
Treated with
Rocephin
Spectinomycin
Treat partner!!
Chlamydia
Three times more common than gonorrhea.
Etiology - Chlamydia trachomatis
Maternal and Fetal Effects
Mom – pelvic inflammatory disease, dysuria,
abortions, pre-term labor
Fetus -- Stillbirth, Chylamydial pneumonia
Interventions
Erythromycin, doxycycline, zithromax
Advise treatment of both partners is very important
Hepatitis A or B
Highly contagious when transmitted by direct contact
with blood or body fluids
Maternal and Fetal Effects:
• All moms should be tested for Hep B during pregnancy
• Fetus may be born with low birth weight and liver changes
• May be infected through placenta, at time of birth, or breast
milk
Intervention:
• Recommend Hepatitis B vaccination to both mother and
baby after delivery.
Rubella
Etiology
Spread by droplet infection or through direct
contact with articles contaminated with
nasopharyngeal secretions.
Crosses placenta
Maternal and Fetal Effects
Mom– fever, general malaise, rash
Most serious problem is to the fetus--causes many
congenital anomalies (cataracts, heart defects)
Intervention
Determine immune status of mother. If titer is low,
vaccine given in early postpartum period
CYTOMEGALOVIRUS
Etiology -- Member of the Herpes virus
• Crosses the placenta to the fetus or contracted during
delivery. Cannot breast feed because transmitted
through breast milk
Effects on Mom and Fetus
• Mom – no symptoms, not know until after birth of the
baby
Fetus -- Severe brain damage; Eye damage
•
Intervention
No drug available at this time
Teach mom should not breast feed baby
Isolate baby after birth
Herpes Simplex Type 2
Maternal and Fetal Effects
Painful lesions, blisters that may rupture and leave
shallow lesions that crust over and disappear in 2-6
weeks
Culture lesions to detect if Herpes, No cure
If mom has an outbreak close to delivery, then
cannot deliver vaginally. Must deliver by Cesarean
birth
*Virus is lethal to fetus if inoculated
at birth
Intervention:
Zovirax
HIV/AIDS
Etiology: Human Immunodeficiency Virus, HIV
Transmission of HIV to the fetus occurs through:
The placenta; birth canal
Through breast milk
**The virus must enter the baby’s
bloodstream to produce infection.
Diagnosis:
ELISA test – identifies antibodies specific to HIV. If positive =
person has been exposed and formed antibodies
Western Blot – used to confirm seropositivity when ELISA is
positive.
Viral load - measures HIV RNA in plasma. It is used to predict
severity – lower the load the longer survival.
CD4 cell count – markers found on lymphocytes to indicate
helper T4 cells. HIV kills CD4 cells which results in impaired
immune system.
Goal: reduce viral load to below 50 copies /ml. and increase
the CD4 cell count.
Nursing Care:
**Provide Emotional Support
**Teach measures to promote wellness
AZT
oral during pregnancy
IV during labor
liquid to newborn for 6 weeks.
**Provide information about resources
Fetal Demise/ Intrauterine
Fetal Death
Assessment:
1. First indication is usually NO fetal
movement
2. NO fetal heart tones
Confirmed by ultrasound
3. Decrease in the signs and symptoms of
pregnancy
Diabetes in Pregnancy
Diabetes creates special problems which affect
pregnancy in a variety of ways.
Successful delivery requires work of the entire health
care team
Endocrine Changes During Pregnancy
There is an increase in activity of maternal
pancreatic islets which result in increase
production of insulin.
Counterbalanced by:
a.
Placenta’s production of Human Chorionic
Somatomammotropin (HCS)
b.
Increased levels of progesterone and
estrogen--antagonistic to insulin
c.
Human placenta lactogen – reduces
effectiveness of circulating insulin
d. Placenta enzyme-- insulinase
Gestational Diabetes
Diabetes diagnosed during pregnancy, but
unidentifable in non-pregnant woman
Known as Type III Diabetes - intolerance to
glucose during pregnancy with return to normal
glucose tolerance within 24 hours after delivery
Glucose tolerance test:
1 hr oral GTT – if elevated, do 3 hour GTT
Gestational diabetes if:
Fasting – 95 mg / dl
1 hour - 180 mg/ dl
2 hour - 155 mg/ dl
3 hour – 140mg/dl
Treatment
Controlled mainly by diet
May use insulin
No use of oral hypoglycemics
Effects of Diabetes on the
Pregnancy
MATERNAL
Increase incidence of
INFECTION
Fourfold greater
incidence of Preeclampsia
Increase incidence of
Polyhydramnios
Dystocia – large babies
Rapid Aging of Placenta
FETAL
increase morbidity
Increase Congenital Anomalies
neural tube defect (AFP)
Cardiac anomalies
Spontaneous Abortions
Large for Gestation Baby, LGA
Increase risk of RDS
Effects of Pregnancy on the Diabetic
Insulin Requirements are Altered
First Trimester--may drop slightly
Second Trimester-- Rise in the requirements
Third Trimester-- double to quadruple by the
end of pregnancy
Fluctuations harder to control; more
prone to DKA
Possible acceleration of vascular
diseases
Interventions/ Nursing Care
Diet Therapy
Insulin Regulation
Blood Glucose Monitoring
Exercise
Monitor Fetal Well Being
Heart Disease in
Pregnancy
Cardiac Response in All Pregnancies
Every Pregnancy affects the cardiovascular system
¤ Increase in Cardiac Output 30% - 50%
¤ Expanded Plasma Volume
¤ Increase in Blood (Intravascular) Volume
A woman with a healthy heart can tolerate the stress of
pregnancy,but a woman with a compromised heart is
challenged Hemodynamically and will have complications
Effects of Heart Disease on
Pregnancy
Growth Restricted Fetus
Spontaneous Abortion
Premature Labor and Delivery
Effects of Pregnancy on
A Diseased Heart
The Stress of Pregnancy on an already weakened
heart may lead to cardiac decompensation (failure).
The effect may be varied depending upon the
classification of the disease
Classification of Heart Disease
Class 1
Uncompromised
No alteration in activity
No anginal pain, no symptoms with activity
Class 2
Slight limitation of physical activity
Dyspnea, fatigue, palpitations on ordinary exertion
comfortable at rest
Class 3
Marked limitation of physical activity
Excessive fatigue and dyspnea on minimal exertion
Anginal pain with less than ordinary exertion
Class 4
Symptoms of cardiac insufficiency even at rest
Inability to perform any activity without discomfort
Anginal pain
Maternal and fetal risks are high
Nursing Care - Antepartum
Decrease Stress
teach the importance of REST!
watch weight
assess for infections - stay away from crowds
assess for anemia
assess home responsibilities
Teach signs of cardiac decompensation
Assess for Signs of CHF
Cough (frequent, productive, hemoptysis)
Dyspnea, Shortness of breath, orthopnea
Palpitations of the heart
Generalized edema, pitting edema of legs and feet
Moist rales in lower lobes, indicating pulmonary edema
Education
Diet
high in iron, protein
low in sodium and calories ( fat )
Weight gain
Medications
Supplemental iron
Heparin, not coumadin – monitor lab work
Diuretics – very careful monitoring
Antiarrhythmics –Digoxin, quinidine, procainamide. *Beta-blockers
are associated with fetal defects.
Reinforce physicians care
Nursing Care: During Labor
• Labor in an upright or side lying position
• Restrict fluids
• On O2 per mask throughout labor and
cardiac monitoring.
• Sedation / epidural given early
• Report fetal distress or cardiac failure
• Stage 2 - gentle pushing, high forceps
delivery
Nursing Care Postpartum
The immediate post delivery period is the
MOST significant and dangerous for the mom
with cardiac problems because:
Following delivery, fluid shifts from extravascular spaces
into the blood stream for excretion
Cardiac output increases, blood volume increases
Strain on the heart! Watch for cardiac failure
Test Yourself !
Mrs. B. has mitral valve prolapse. During the
second trimester of pregnancy, she reports fatigue
and palpitations during routine housework. As a
cardiac patient, what would her functional
classification be at this time?
a. Class I
b. Class II
c. Class III
d. Class IV