Transcript Hyper / Hypo Disorders

Spring 2012
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, PIH
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
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




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

(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 anticoagulant) is produced

Fibrinogen fibrin which enhances platelet aggregation and clot
formation

Widespread fibrin and platelet deposition in capillaries and
arterioles
 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
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 = Systolic 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 = other signs plus convulsions not
attributable to other causes
Chronic HTN = BP > or equal to 140/90 that was
known to exist before pregnancy or does not
resolve after 6 weeks after delivery
Predisposing Factors
 Primigravida
 Multiple gestation pregnancy
 Vascular Disease
 Age >35
 Obesity
PATHOLOGICAL CHANGES
PIH is 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 PIH 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 cc. /
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
 Hyper-reflexia
 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
Pre-Eclampsia
Mild
Severe
 140/90
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 Protien 1+ to 2+
 Edema 1+ to lower legs
 < 1lb/ week
 Reflexes 1+ to 2+
160/90
Protein 3+ to 4+
Edema 3+ to 4+
>2 lb/ week
Reflexes 3+ to 4+ (hyperreflexia)
Clonus present
Blurred vision or Scotoma
Retinal detachment
N&V, Epigastric pain
Elevated Liver enzymes
Headache or change in LOC
Premature aging of placenta,
IUGR, & or late decelerations
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 reflexes for hypo-reflexia -- D/C if hypo-refexia
3. Measure Urinary Output >100cc in 4 hrs.
4. Measure Magnesium levels – normal is 1.5-2.5 mg/dl
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 PIH
 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 a
form of severe preeclampsia eclampsia
 H = hemolysis of RBC
 EL = elevated liver enzymes
 LP = low platelets <100,000mm
(thrombocytopenia)
Etiology
of
HELLP
Hemolysis occurs from destruction of RBC’s
Release of bilirubin
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. Right upper quadrant pain and tenderness
2. Nausea and vomiting
3. Edema
4. Flu like symptoms
5. Lab work reveals –
a. anemia – low Hemoglobin
b. thrombocytopenia – low platelets. < 100,000.
c. elevated liver enzymes:
-AST asparatate aminotransferase (formerly
SGOT) exists within the liver cells and with
damage to liver cells, the AST levels rise > 20 u/L.
- LDH – when cells of the liver are lysed, they spill
into the bloodstream and there is an increase in
serum > 90 u/L/
HELLP
 Intervention:
 1. Bedrest – any trauma or increase in intra-
abdominal pressure could lead to rupture
of the liver capsule hematoma.
 2. Volume expanders
 3. Antithrombic medications
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
 T O R C H A Infections
T = Toxoplasmosis
O = Other
Syphilis, Gonorrhea,
Chlamydial,Hepatitis A or B
R = Rubella
C = Cytomegalovirus
H = Herpes
A = Aids
 Toxoplasmosis
Etiology
Protozoan infection. Raw meat and cat litter
Maternal and Fetal Effects
 Mom - flu-like symptoms, lymphadenopathy
 Fetus – still, 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
MATERNAL
Effects of Diabetes on the
Pregnancy
 Increase incidence of
INFECTION
 Fourfold greater incidence of
Pre-eclampsia
 Increase incidence of
Polyhydramnios
FETAL
 increase morbidity
 Increase Congenital Anomalies
 neural tube defect (AFP)
 Cardiac anomalies
 Spontaneous Abortions
 Dystocia – large babies
 Rapid Aging of Placenta
 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