Ob Exam 2

Front 1

Fetal Heart Rate Mechanisms

Back 1

1. Parasympathetic System (cardiodecelerator)
2. Sympathetic System
(cardioaccelerator)
3. Baroreceptors
(decrease in fetal heart rate)
4. Chemoreceptors
(Respond to a drop in fetal oxygen by increasing HR. If prolonged- decreases HR.)

Front 2

Parasympathetic System for fetal monitoring

Back 2

Cardiodecelerator
Vagus nerve is primary nerve
As fetus matures PS becomes more dominant (HR decreases)

Front 3

Sympathetic System (for fetal monitoring)

Back 3

Cardioaccelerator
Nerve endings are distributed throughout the heart muscle.
When stimulated they release norepinephrine.
Increases heart rate and strength of cardiac contractions, increasing CO

Front 4

Baroreceptors (for fetal monitoring)

Back 4

(decrease in fetal heart rate)
In the carotid arteries and in the walls of the major arteries
Fetal BP increases as a result of increase in intervascular volume.
Example: Compression of umbilical arteries- stimulates baroreceptors, sends impulse ot vagus nerve causing decrease in heart rate

Front 5

Chemoreceptors (for fetal monitoring)

Back 5

Respond to a drop in fetal oxygen by increasing HR. If prolonged- decreases HR.
In medulla oblongata (in brain stem)
Respond to changes in pH, O2 and CO2 levels in the blood.
Respond to drop in O2 (hypoxia) with an increase in the heart rate as an attempt to get O2 to the brain, but if it continues it stimulates the baroreceptors which then stimulare the vagus nerve decreased in HR

Front 6

Baseline Rate for FHR and how to you get the number

Back 6

110-160 bpm
The average FHR during a 10 minutes period, rounded to increments of 5 bpm

Front 7

Internal uterine pressure catheter

Back 7

Intran or IUPC
Very accurate about how strong contraction is.
Used when not getting a good tracing with the external or if you want to know if contractions are strong enough.
Can help monitor effects of pitocin

Front 8

Evaluation of Fetus (how often per stage)

Back 8

1st stage: Low Risk- q 30 min High Risk- q 15 min
2nd stage: Low Risk- q 5-15 min
High Risk- q 5 min

Front 9

Tachycardia in fetus and causes

Back 9

over 160 bpm x 10 min
Can be an ominous signs if w decreased variability, late decels or severe variable decels
Reasons: fetal stress and early fetal hypoxia, maternal fever, if mother receives cardiac stimulating drugs (tributiline, atropine) maternal hyperthyroidism (maternal hormones cross placenta) dehydration, anxiety, prematurity, fetal anemia

Front 10

Bradycardia in fetus and causes

Back 10

less than 110 bpm x 10 min
Ominous w decreased variability and/or late decels
Reasons: Late fetal hypoxia (fetal asphyxia), maternal hypotension, umbilical cord compression (when fetal baroreceptors are stimulated)

Front 11

Baseline Variability (in fetus) breakdowns

Back 11

Absent- range undetected
Minimal- range 5 bpm
Moderate- range of 6-25 bpm
Marked- range greater than 25 bpm

Good indicator of fetal cardiac and neurological function

Front 12

Absent Variability in Fetal Monitoring

Back 12

range undetected
almost a flat line

Front 13

Minimal Variability in Fetal Monitoring

Back 13

A range of 5 bpm

Front 14

Moderate Variability in Fetal Monitoring

Back 14

Range of 6-25 bpm

Front 15

Marked Variability in Fetal Monitoring

Back 15

Range greater than 25 bpm

Front 16

Sinusoidal pattern

Back 16

Smooth wavelike baseline that is equally distributed above and below baseline.
Amplitude is between 5 & 15
Baby is in danger. Associated with sinusoidal pattern
Pseudo- if given drugs like morphine or demerol

Front 17

What are the two kinds of accelerations? What are the requirements for < or > 32 weeks?

Back 17

Increase in HR ---
Episodic accelerations: with movement or from external stimulation
&
Periodic accelerations: with UCs
These are reassuring signs

After 32 weeks gestation- Must be 15 beats above BL for 15 seconds

(Less than 32 weeks- 10 beats above BL for 10 seconds)

Front 18

Episodic accelerations

Back 18

with movement or from external stimulation

Front 19

Periodic accelerations

Back 19

with UCs

Front 20

Early Decelerations

Back 20

from pressure on fetal head

Timing with UCs, greater than 30 seconds to reach nadir (bottom/deepest part).
They 'mirror' the contractions

Will see with pushing. Pushing on head stimulates vagus nerve

Front 21

Late Decelerations

Back 21

uteroplacental insufficiency

Greater than 30 seconds to reach nadir, nadir after peak of UC

Front 22

Variable Decelerations

Back 22

umbilical cord compression

15 bpm below BL X 15 seconds, less than 30 seconds to reach nadir.
May have 'u' 'v' or 'w' with fast drops
Intervention: first try turning the mother

Front 23

Prolonged Decelerations

Back 23

FHR decrease is 15 bpm or more and lasts for at least 2 minutes but less than 10 minutes

Hint 23

Generally- the baby is losing all reserves

Once you go past 10 min- it's just bradycardia

Front 24

Ultrasound

Back 24

Sound waves are sent
through maternal
abdomen and bounce off
of fetal heart valve.
Heart rate is interpreted
by monitor. Best when
placed over fetal back.

Front 25

Internal Fetal Scalp Electrode

Back 25

Placed onto fetal scalp
Gives ECG reading
Placed by nurse, midwife, or physician

Front 26

Amnioinfusion

Back 26

add fluid into the uterus to help get baby up off the cord or sometimes when baby has passed meconium
for cord compression

Front 27

Tocometer

Back 27

Pressure sensitive button indicates contraction of uterine muscle

Not useful for determining strength of contraction

Best recording often obtained when positioned at fundus (top of uterus)

Front 28

Internal Uterine Pressure Catheter

Back 28

Accurately tells us how strong the contractions are

Front 29

To calculate Montevideo Units (MVU)

Back 29

After IUPC insertion, measure units of pressure above baseline
Multiply units of pressure by number of UC’s in 10 minutes
Example: If uterine pressure is 50 mmHg and the patient has 3 UC’s in 10 mins, total Montevideo units (MVUs) would be equal to 150 MVUs.
Usually 200 MVUs is considered necessary for adequate labor during the active phase.

Front 30

Scalp Stimulation

Back 30

An indirect method of assessing fetal acid base balance when no accelerations on monitor
Stimulation to the fetal scalp with finger
Reactivity is associated with fetal well-being
Basically a vag exam where you rub the baby's head

Front 31

Fetal Blood Sampling

Back 31

Fetus is well oxygenated if pH stays above 7.25
Continue monitoring and resample if pH heads downward and is between 7.25 and 7.20
Below 7.20 shows fetus is acidotic. Prepare for birth

Front 32

Ultrasound
what can u see?
2 types

Back 32

High frequency soundwaves
placental location, fetal number, assessment of gestation age, assessment of amniotic fluid (AFI)- how much?,
Transabdominal- woman needs to fill bladder before the procedure (drinks water 1-2 hors before appointment
Transvaginal- probe goes up vagina, images tend to be more clear, mother may have an empty bladder

Front 33

BPP Test Interpretation and Management
10/10
8/10

Back 33

10/10 Normal nonasphyxiated fetus.
No intervention. Repeat in 1 week.
8/10 With normal fluid:
Risk of fetal asphyxia very rare.No intervention.
With abnormal fluid:
Chronic fetal asphyxia suspected. Induce birth.

Front 34

BPP Test Interpretation and Management
6/10
4/10

Back 34

6/10 Possible fetal asphyxia. If AFV is abnormal, deliver otherwise repeat test.
4/10 Probable fetal asphyxia. Repeat testing same day

Front 35

BPP Test Interpretation and Management
2/10
0/10

Back 35

2/10 Almost certain fetal asphyxia. Induce birth
0/10 Certain fetal asphyxia. Induce birth

Front 36

NonStress Test (NST)

Back 36

Reactive NST- 2 or more accelerations, 15 bpm or more, lasting 15 seconds or longer, within a 20 minute period. (If under 32 weeks gestation- an acme of 10 bpm or more, for 10 seconds or longer.)

Nonreactive NST- does not meet the above criteria

Front 37

Contraction Stress Test (CST)

Back 37

Evaluates uteroplacental functioning. Typically given after a nonstress test
Need 3 uterine contractions 40-60 secs in duration in 10 min.
Use pitocin or strumming technique (strum nipple to release oxytocin)
Negative CST- No late decels or significant variable decels after any UCs.
Positive CST- Late decels with at least 50% of UCs.

Front 38

Amniocentesis

Back 38

Use ultrasound
22 gauge spinal needle
Draw up small amount of amnio fluid
Chromosomal
Biochemical determination
AFP alpha fetal protein
Lung Maturity

Front 39

AFP- Alfa fetal protein

Back 39

protein produced in fetal liver
peaks at about 15 wks in amniotic fluid, found with women who's babies have neural tube defects

Front 40

Lung Maturity Studies

Back 40

1. L/S Ratio (Lecithin/Sphingomyelin)
lungs are mature when ratio 2:1

2. PG (Phosphatidylglycerol)

Front 41

L/S Ratio (Lecithin/Sphingomyelin)

Back 41

The surfactant is made up of lecithin/sphingomyelin.
When ratio is 2:1 there is high likelihood of maturity
@ 20 wks 0.5:1

Front 42

PG (Phosphatidylglycerol)

Back 42

2nd most abundant phospholipid in surfactant
Appears around 36 wks gestation
It’s either present or abset. When it’s present the lungs are mature

Front 43

Chorionic Villus Sampling (CVS)

Back 43

done for diagnosis of genetic, metabolic or dna studies
done between 10-12 wks gestation
Aspirate a small amount of chorionic villus from edge of placenta
Can cause bleeding or rupture of amniotic fluid

Front 44

Fetal Development at 8 Weeks

Back 44

All body organs are formed

Front 45

Fetal Development at 8-12 Weeks

Back 45

FHT’s can be heard with doppler

Front 46

Fetal Development at 16 Weeks

Back 46

Baby’s sex can be seen. Looks like a baby.

Front 47

Fetal Development at 20 Weeks

Back 47

Quickening, baby develops regular schedule, vernix, head hair, eyebrows, and eyelashes present

Front 48

Fetal Development at 24 Weeks

Back 48

Weighs 1 lb/10 oz. Activity is increasing.

Front 49

Fetal Development at 28 Weeks

Back 49

Eyes begin to open and close. Baby is 2/3s its final size.

Front 50

Fetal Development at 32 Weeks

Back 50

Baby has fingernails and toenails. SQ tissue is being formed. Baby is less wrinkled and red.

Front 51

Fetal Development at 38-40 Weeks

Back 51

Baby fills total uterus.

Front 52

Tobacco effects on Men and Women

Back 52

higher infertility rates
Men have impaired sperm concentration and changes in sperm motility
Women have difficulties with ovulation and implant disorders (too low in uterus)

Front 53

Tobacco effects on fetus/infants

Back 53

Infants have a lower birth weight and a higher incidence of perinatal deaths
Infants born to smokers are more than twice as likely to die from SIDS
Increased risk of spontaneous abortion, preterm birth, placenta previa, abruptio placenta, and premature rupture of membranes

r/t amount of cigarrettes Nicotine and Carbon Monoxide decrease amount of O2 available for the baby

Front 54

Risks to the Fetus of the Drug Dependent Mother

Back 54

Intrauterine anoxia
Intrauterine infection
Alterations in birth weight
Low Apgar scores

Front 55

The Female Addict

Back 55

Problems with criminality (selling self) and physical abuse

stay away from pregnant hookers

Front 56

What happens when mother goes through withdrawal?

Back 56

baby does too -causing hyperactivity and you may see cord around neck

Front 57

Many drugs during pregnancy increase risk for

Back 57

many drugs increase risk for pregnancy induced HTN (PIH) and abruptio placenta that result in placental insuffiency and fetal anoxia

Front 58

The Effect (on the fetus) of a Substance is Determined by:

Back 58

1. The stage of fetal development
2. The amount of substance taken
3. The type of substance taken

Front 59

Identifying the Substance Abuser- Obstetric History

Back 59

In prior pregnancies, a history of:
-Abruptio placenta
-Fetal death (after 20 wks)
-Low-birthweight infant
-Meconium staining
-Premature rupture of membranes
-Premature labor
-Sexually transmitted diseases
-Spontaneous abortion

Front 60

What does Cocaine and other Stimulants do to the body?

Back 60

Stimulants act at the nerve terminals to prevent the reuptake of dopamine and norepinephrine, which results in vasoconstriction, tachycardia, and hypertension.

Placental vasoconstriction decreases blood flow to the fetus

Front 61

What are the effects of Cocaine and other Stimulants on the fetus?

Back 61

Placental abruption
Low birth weight (IUGR)
Marked irritability of the newborn
Increased risk of SIDS

Front 62

Heroin effects on infant

Back 62

Fetal death can occur when addicted mothers stop usage suddenly
Low birth weight
Deficits in cognitive and developmental testing
The most harmful effect on the newborn is withdrawal- neonatal abstinence syndrome

Front 63

Signs of Neonatal  Withdrawal (NAS)

Back 63

W - wakefulness
I - irritability
T - tremulousness, temperature variation, tachypnea
H - hyperactivity, high-pitched cry, hyperreflexia, hypertonus, hiccups
D - diarrhea, diaphoresis, disorganized suck
R - rub marks on knees, elbows, and face
A - apneic spells
W - weight loss (or failure to gain weight)
A - alkalosis (respiratory)
L - lacrimation
S - stuffy nose, sneezing, seizures

Front 64

Caring for the Drug-Affected infant

Back 64

For Frantic Crying: dark quiet room, swaddle baby, pacifier, rock baby gently
For Tremors: swaddle and hold close, provide firm, gentle touch
to tremulous area

Front 65

Fetal Alcohol Syndrome Incidence

Back 65

The incidence is between 2-15 cases per 10,000 live births in the United States.
FAS is the leading cause of mental retardation in the western world.
The average I.Q. is 74.
NO amount of alcohol is safe during pregnancy!

FASD= 1 in 100 births in U.S.

Front 66

Clinical Characteristics of Fetal Alcohol Syndrome (FAS)

Back 66

Growth Deficiencies
Central Nervous System Involvement
Facial Dysmorphology

Front 67

Growth Deficiencies in FAS

Back 67

Failure to thrive
Low birth weight
Micorcephaly (small head & brain)
Short and thin for age

Front 68

Central Nervous System Involvement in FAS

Back 68

Developmental delay
Hyperactivity
Learning or attention disorders
Motor incoordination
Mental retardation

(need at least 1)

Front 69

Facial Dysmorphology in FAS

Back 69

Epicanthal folds
Flat nasal bridge
Flat and elongated philtrum (bump between lips and nose)
Thin upper lip
Short palpebral fissures
Upturned nose

Front 70

Intrauterine Growth Restriction (IUGR)

Back 70

Advanced gestation and limited fetal growth
Considered an “undergrown newborn”
Aka- small for gestational age SGA
Baby will be in less than 10%

Front 71

Factors Contributing to IUGR

Back 71

Maternal factors- ie low socioeconomic status, lack of prenatal care, and malnutrition
Maternal disease- ie substance abuse, heart disease, preeclampsia
Envirnomental factors- ie high altitude, excessive exercise, maternal use of teratogenic drugs
Placental factors- ie small placenta, placenta previa
Fetal factors- ie congenital infections, chromosome abnormalities
(Low socioeconomic- effects health, how they take care of themselves)

Front 72

Symmetric (proportional) IUGR

Back 72

caused by long term conditions that affect the fetus (malnutrition, chronic HTN, chronic drug use)
See a shorter lighter baby and small organs and everything.baby is less than 10

Front 73

Asymmetric (disproportional) IUGR

Back 73

later in pregnancy with uteral placental blood flow (preeclampsia) the head circumference and length are appropriate but still under 10%

Front 74

Small for Gestational Age (SGA)

Back 74

A SGA newborn can be preterm, term, or postterm

Less than 2 standard deviations or less than the 10th percentile for weight

Front 75

Complications of the SGA Newborn

Back 75

Chronic Hypoxia (Asphyxia)
Aspiration Syndrome
Hypothermia
Hypoglycemia
Polycythemia

Front 76

Chronic Hypoxia (asphyxia) in SGA Newborn occurs because

Back 76

occurs because they don't tolerate labor well.

Front 77

Aspiration Syndrome in SGA Newborn occurs because

Back 77

Meconium in the amniotic fluid is aspirated at birth

Front 78

Hypothermia in SGA Newborn occurs because

Back 78

Have less brown fat and less adipose tissue so they lose heat very easily after birth
Brown fat- newborns are born with it in armpits, abdomen and fat, only lasts a few weeks. They don’t have the ability to shiver. So they are born with the brown fat- if they get too cold they metabolize the fat and it heats them up

Front 79

Hypoglycemia in SGA Newborn occurs because

Back 79

Because they have less glycogen stores
Because they have increased metabolic rate from heat loss

Front 80

Polycythemia in the SGA Newborn occurs because

Back 80

The body starts to produce more red blood cells due to chronic hypoxia in utero.
Can lead to jaundice
Do a partial exchange transfusion if it’s pretty significant. So some blood is removed but replaces ml by mL with plasma or plasmanate or 5% albumin (not tested)

Front 81

Compare normal newborn hemoglobin and hematocrit levels to that with polycythemia

Back 81

Normal
Hemoglobin- 15-22g/dl
Hematocrit - 50%-65%

Polycythemia
Hemoglobin- greater than 22g/dl
Hematocrit- greater than 65%-70%

Front 82

Biggest problem in premature infants

Back 82

Respiratory Distress Syndrome

Front 83

Respiratory Distress Syndrome in premature infants

Back 83

b/c of immaturity of lungs
Before this time they have inability to produce enough surfactant (keeps alveoli open)
These babies usually end up in NICU on oxygen
Tire out with feeds so you use a gavage tube

Front 84

Loss of Heat
Non-shivering thermogenesis in newborn

Back 84

Very little subQ fat.
Baby’s posture makes a difference. Conserve heat when in kind of fetal position
Greater risk for aspiration because gag relfex is not developed
Thermogenesis- is the break down of the brown fat, which is used up within a few weeks

Front 85

Kernicteris

Back 85

what you prevent by treating jaundice. All the bilirubin does into the brain and causes brain damage & mental retardation and nerve damage (irreversible), baby gets lethargic and loses ability to suck, if progresses then see vomiting and loss of moro reflex. Bili level above 20-25 and whole body yellows. Become irritable, hypertonic, and has seizures

Front 86

3 Types of Jaundice

Back 86

Physiological
Breast Milk
Pathologic

Front 87

Physiological Jaundice

Back 87

Most common, Always cover eyes. Will see 2-3 days after birth
Caused by destruction of RBC’s and impaired conjugation of bilirubin in the immature liver
For the bilirubin to get out of baby’s body it must go through conjugation process. Goes from ‘indirect’ to ’direct’ so it can go out of bowels. Sunlight can do it.
If baby has cephalhematoma more concerned with jaundice because the blood must be absorbed into the body- increase of bilirubin that must be processed
Forceps baby, bruising on face
50% of full term babys have problem
80% of preterm
Do blood draw to get bili level
if higher than 12 in term bottle fed baby, 14 in term breastfed baby and 15 in preterm- considered jaundice
Starts in head, as number gets high than goes down the rest of the body

Front 88

Breast Milk Jaundice

Back 88

Bili levels increase after 1st week of life and peak at 2-3 weeks.
Some women’s breast milk contains more free fatty acids, they complete with bilirubin for the binding sites on albumin
Stop breastfeeding for 2-3 days, baby goes on formula to allow break of cycle
Then resume breastfeeding

Front 89

Pathologic Jaundice

Back 89

Most dangerous
Suspected when the yellow discoloration is visible before 24 hours of life in term infant
Before 48 hours in the preterm infant
Bilirubin levels are generally above 12 and 14.

Front 90

ABO Incompatability

Back 90

Mother Fetus
0 / A or B
A / B
B / A

Hemolytic condition that occurs when the major blood group of the mother is incompatible with that of the fetus.
Maternal antibodies are formed against cells of fetus’s blood type
Maternal antibodies are found on fetal RBC, those antibodies cause clumping (agglutination) of fetal RBCs the clumps get in small blood vessels where they hemolyze or are broken down and causes an increase in bilirubin
Can get severe hyperbilirubinemia or renal failure
Clinical Indicators: See neonatal jaundice within 24 hrs of life and get something called Direct Coombs Test, will detect presece of maternal antibodies in neonates blood. If present = positive direct coombs test
Tx: phototherapy or exchange transfusion

Front 91

RH Incompatibility

Back 91

Causes a hemolytic disease in fetus/newborn
Occurs when mother is Rh neg and baby is Rh positive
The fetal red blood cells contain d-antigens, the mother does not
They get into the mothers body
During the birth there is a mixing and baby’s blood gets into the mother
The mother create antibodies that will cross the placenta and attack the next baby if she does not receive Rhogam (destroys RBCs from baby that get into her system)
It’s called erythroblastosis fetalis causing fetal anemia
If severe- hydrops fetalis: continuation of the erythroblastosis fetalis, baby gets edematis and can cause CHF and multisystem failure and death in utero

Front 92

Diaphragmatic Hernia

Back 92

results from defect in baby’s diaphragm. Allows abdominal organs to be displaced so the intestines get into the thoracic cavity cause lungs to remain small. Usually on the left side. Most are discovered with ultrasound. Severe Respiratory Distress at birth.
Will see a scaffoid abdomen (flat or dipped) barrel chest. An x-ray will show loops of intestines
Do not bag the baby because air will go into the stomach. You want to put in an endotracheal tube and put the baby on a ventilator.A gastic tube into stomach to relieve any air. Position in High Semi-fowlers position or turn onto affected side.

Front 93

Biophysical Profile (BPP)

Back 93

Biophysical Profile
-fetal breathing movements
-gross body movements
-fetal tone
-qualitative amniotic fluid volume
-reactive FHR