The document discusses various methods for evaluating fetal lung maturity prior to delivery, including quantifying pulmonary surfactant components in amniotic fluid. The lecithin/sphingomyelin (L/S) ratio is the most common approach, where an L/S ratio of 2.0 or greater indicates maturity. Phosphatidylglycerol (PG) appears at 35 weeks and further ensures lung maturity. Tests help determine the risks of respiratory distress syndrome and guide management decisions.

2.  The number of late fetal deaths (fetal deaths of 28
weeks' gestation or more) plus early neonatal
deaths (deaths of infants 0 to 6 days of age) per
1,000 live births.
 A live birth is the complete expulsion or extraction
of a product of conception from its mother,
irrespective of the duration of the pregnancy, that,
after separation, breathes or shows any evidence of
life, such as beating of the heart, pulsation of the
umbilical cord, or definite movement of voluntary
muscles, whether or not the umbilical cord has
been cut or the placenta is attached; each product
of such a birth is considered live born

3.  Fetal deaths may be divided into those that occur
during the antepartum period and those that occur
during labor, intrapartum stillbirths.
 From 70%-90% of fetal deaths occurred before the
onset of labor.
 Point out that antepartum deaths may be divided
into four broad categories:
◦ (1) chronic asphyxia of diverse origin;
◦ (2) congenital malformations;
◦ (3) superimposed complications of pregnancy, such as Rh
isoimmunization, placental abruption, and fetal infection;
and
◦ (4) deaths of unexplained cause.
 If it is to succeed, a program of antenatal
surveillance must identify malformed fetuses and
recognize those at risk for asphyxia.

4.  In summary, based on available data, approximately
◦ 30 percent of antepartum fetal deaths may be attributed to
asphyxia (IUGR, prolonged gestation),
◦ 30 percent to maternal complications (placental abruption,
hypertension, preeclampsia, and diabetes mellitus),
◦ 15 percent to congenital malformations and chromosomal
abnormalities, and
◦ 5 percent to infection.
◦ At least 20 percent of stillbirths have no obvious etiology,
and this percentage increases with advancing gestational
age.
◦ That is, late gestation stillbirths are more likely to have no
identifiable etiology
 A large clinical experience has demonstrated that
antepartum fetal assessment can have a significant
impact on the frequency and causes of antenatal fetal
deaths

5.  Aspects of Fetal Condition That Might
be Predicted by Antepartum Testing
◦ Perinatal death Intrauterine growth
restriction (IUGR)
◦ Nonreassuring fetal status, intrapartum
◦ Neonatal asphyxia Postnatal motor and
intellectual impairment
◦ Premature delivery
◦ Congenital abnormalities Need for specific
therapy

6.  Testing can be initiated at early
gestational ages, 25 to 26 weeks, to
identify the fetus at risk.
 Maternal and fetal interventions can
then be considered
 Antepartum fetal testing can more
accurately predict fetal outcome than
antenatal risk assessment using an
established scoring system.

7.  The near-term fetus spends approximately
25% of its time in a quiet sleep state (state
1F) and 60-70% in an active sleep state
(state 2F)
 Active sleep is associated with rapid eye
movement (REM). In fetal lambs,
electrocortical activity during REM sleep is
characterized by low-voltage, high-
frequency waves

8.  In conclusion, there is a clearly established
relationship between decreased fetal activity
and fetal death. Therefore, it would seem
prudent to request that all pregnant patients,
regardless of their risk status, monitor fetal
activity starting at 28 weeks' gestation. The
Count-to-Ten approach developed by Moore
and Piacquadio seems ideal.
 Maternal assessment of fetal activity is a
valuable screening test for fetal condition.
 Should the mother report decreased fetal
activity, an NST is performed. In this
situation, most NSTs are reactive.

9.  ACOG Bulletin #9: Antepartum Fetal
Surveillance goal is to prevent fetal death
through detection of hypoxic or acidemic
infant,Not predictive of acute events like cord
accident or abruption
 Non reactive NST have cord pH 7.28, cessation
of movement 7.16
Fetal Movement (Kick Counts)
 several protocols, no ideal
 generally 10 movements in 2 hours considered
reassuring

10.  3/10 ‘/40”, either spon or induced w/ pitocin is administered by
an infusion pump at 0.5 mU/min. The infusion rate is doubled
every 20 minutes until …or nipple stim
 -nipple stim induces ctx in less time than oxytocin infusion
 -interpreted according to presence or absence of late decels
 -Neg: no late or sig variables
 -Pos: late decels following 50% or more of ctx
 -Equivocal-suspicious: int late decels or sig variables
 -Equivocal-hyperstim:decels in presence of ctx more
frequent than q 2min or lasting > 90 s
 -Unsatisfactory: <3 ctx in 10 min or uninterpretable tracing
 -relative contraindication: PTL or high risk of PTL, PPROM, prev
classical c/s or extensive uterine surgery, known placenta previa
 (A positive test would be any 10-minute segment of the tracing
that includes three contractions, all showing late decelerations)
 A CST with both a positive and negative window would be
interpreted as positive.

11.  Variable decelerations that occur during the CST may indicate
cord compression often associated with oligohydramnios
 A negative CST has been consistently associated with good
fetal outcome.
 Therefore, a negative result permits the obstetrician to
prolong a high-risk pregnancy safely
 A positive CST has been associated with an increased
incidence of intrauterine death, late decelerations in labor, low
5-minute Apgar scores, IUGR, and meconium-stained
amniotic fluid
 There is no doubt that the high incidence of false-positive
CSTs is one of the greatest limitations of this test, because
such results could lead to unnecessary premature
intervention.
 False-positive CSTs may be attributable to misinterpretation
of the tracing; supine hypotension, which decreases uterine
perfusion; uterine hyperstimulation, which is not appreciated
using the tocodynamometer; or an improvement in fetal
condition after the CST has been performed
 A suspicious or equivocal CST should be repeated in 24 hours

12.  -HR should temp accel w/ fetal movement
 -loss of reactivity in acidotic, neurologically depressed
or sleeping fetus
 -accels of 15 by 15
 -reactive:2 or more accels in 20 min period
 -nonreactive: lacks accels over 40 min period
 -from 28-32 wks 15% nonreactive in nl fetus
 -variables in 50%, if nonrepetitive and brief no need
for intervention
 The most widely applied definition of a reactive test
requires that at least two accelerations of the fetal
heart rate of 15 bpm amplitude and 15 seconds'
duration be observed in 20 minutes of monitoring
 CNS depressants such as narcotics and phenobarbital,
as well as the b-blocker propranolol, can reduce heart
rate reactivity

13.  The NST has proved to be an ideal screening
test and remains the primary method for
antepartum fetal evaluation at most centers.
 It can be quickly performed in an outpatient
setting and is easily interpreted.
 In contrast, the CST is usually performed near
the labor and delivery suite, may require an
intravenous infusion of oxytocin, and may be
more difficult to interpret.

14. ”Fetal breathing movements were the first biophysical
parameter to be assessed using real-time
ultrasonography.
It is thought that the fetus exercises its breathing muscles in
utero in preparation for postdelivery respiratory
function(swallowing of amionitic fluid).
With real-time ultrasonography, fetal breathing movement
(FBM) is evidenced by downward movement of the
diaphragm and abdominal contents, and by an inward
collapsing of the chest.
Fetal breathing movements become regular at 20 to 21
weeks and are controlled by centers on the ventral
surface of the fourth ventricle of the fetus.
They are observed approximately 30 percent of the time,
are seen more often during REM sleep, and, when
present, demonstrate intact neurologic control.
Although the absence of FBMs may reflect fetal asphyxia,
this finding may also indicate that the fetus is in a period
of quiet sleep.

15.  Fetal breathing movements
◦ 2-At least one episode of >30 seconds' duration in 30 minutes' observation
◦ 0-Absent or no episode of ≥30 seconds' duration in 30 minutes
 Gross body movement
◦ 2-At least three discrete body/limb movements in 30 minutes (episodes of
active continuous movement considered a single movement)
◦ 0-Up to two episodes of body/limb movements in 30 minutes
 Fetal tone
◦ 2-At least one episode of active extension with return to flexion of fetal
limb(s) or trunk, opening and closing of hand considered normal tone
◦ 0-Either slow extension with return to partial flexion or movement of limb in
full extension or absent fetal movement
 Reactive fetal heart rate /non stresss test
◦ 2-At least two episodes of acceleration of ≥15 bpm and 15 seconds/duration
associated with fetal movement in 30 minutes
◦ 0-Fewer than two accelerations or acceleration <15 bpm in 30 minutes
 Qualitative anmiotic fluid volume
◦ 2-At least one pocket of amniotic fluid measuring 2 cm in two perpendicular
planes
◦ 0-Either no amniotic fluid pockets or a pocket <2 cm in two perpendicular
planes

16.  NST, breathing movements (episode(s) of 30
sec in 30 min),
 fetal movement(3 or more discrete
movements in 30 min),
 fetal tone (one or more extension w/ rtn to
flex or opening/closing of hand),
 AFI (single vertical pocket >2cm)
 8/10 nl,
 6/10 equivocal,
 4/10 less or abnorma

17. 10 Normal infant;
 low risk of chronic aphyxia Repeat testing at weekly intervals; repeat
twice weekly in diabetic patients and patients at 41 weeks' gestation
8 Normal infant;
 low risk of chronic aphyxia Repeat testing at weekly intervals; repeat
testing twice weekly in diabetics and patients at 41 weeks'
gestation; oligohydramnios is an indication for delivery
6 Suspect chronic asphyxia
 If 36 weeks' gestation and conditions are favorable, deliver; if at
>36 weeks and L/S <2.0, repeat test in 4–6 hours; deliver if
oligohydramnios is present
4 Suspect chronic asphyxia
 If 36 weeks' gestation, deliver; if <32 weeks' gestation, repeat score
0–2 Strongly suspect chronic asphyxia
 Extend testing time to 120 minutes;
 if persistent score ≤4, deliver, regardless of gestational age

18.  NST was needed in less than 5 percent of tests.
 however, the NST allows the detection of fetal heart
rate decelerations.
 In the presence of reduced amniotic fluid, these
decelerations may be associated with a cord accident.
 drawbacks of the BPP
◦ Ultrasound machine is required, and unless the BPP is
videotaped, it cannot be reviewed.
◦ If the fetus is in a quiet sleep state, the BPP can require a
long period of observation.
◦ The present scoring system does not consider the impact of
polyhydramnios .
 BPP is most commonly used as the final backup test
in the NST and CST sequence of testing and is
critically important when dealing with the premature
fetus

19.  AFI and NST only
 -in 2nd and 3rd trimester AF reflects urine and may indicate placental
dysfunction
 Umbilical Artery Dopplers
 -in cases of severe IUGR see reversed or absent diastolic flow
 Clinical Considerations
 -dearth of evidence that current surveillance decr fetal death from
RCTs
 -use in pregnancies where incr risk of fetal demise
 -initiate testing 32-34 wks for most pts, if mult or very worrisome
start 26-28 wks
 -interval of weekly to twice weekly depending on severity of condition
 patients with diabetes mellitus, IUGR, or a prolonged gestation are
tested twice weekly.
 -interpret results in context of overall clinical picture
 -no single test is considered superior
 -dopplers only useful in setting of IUGR
 Flow chart for antepartum fetal surveillance in which the NST and AFI
are used as the primary methods for fetal evaluation. A nonreactive
NST and decreased AF are further evaluated using either the CST or the
BPP

20.  RDS is caused by a deficiency of pulmonary surfactant, an
antiatelectasis factor that is able to maintain a low stable surface
tension at the air-water interface within alveoli. Surfactant decreases
the pressure needed to distend the lung and prevents alveolar collapse
(see Chapter 20 ). The type II alveolar cell is the major site of surfactant
synthesis.
 Surfactant is packaged in lamellar bodies, discharged into the alveoli,
and carried into the amniotic cavity with pulmonary fluid.
 Phospholipids account for more than 80 percent of the surface active
material within the lung, and more than 50 percent of this phospholipid
is dipalmitoyl lecithin. The latter is a derivative of glycerol phosphate
and contains two fatty acids as well as the nitrogenous base choline.
 PG is the second most abundant lipid in surfactant and significantly
improves its properties
 Other phospholipids contained in the surfactant complex include
phosphatidyl-glycerol (PG), phosphatidyl-inositol, phosphatidyl-serine,
phosphatidyl-ethanolamine, sphingomyelin, and lysolecithin.

21.  Available methods for evaluating fetal
pulmonary maturity can be divided into three
categories:
(1) quantitation of pulmonary surfactant, such as the
lecithin/sphingomyelin (L/S) ratio;
(2) measurement of surfactant function including the
shake test; and
(3) evaluation of amniotic fluid turbidity.
 The first category has become the most
common and reliable in current practice

22. Lecithin/Sphingomyelin Ratio
 The amniotic fluid concentration of lecithin increases
markedly at approximately 35 weeks' gestation, whereas
sphingomyelin levels remain stable or decrease.
 Rather than determine the concentration of lecithin that
could be altered by variations in amniotic fluid volume,
Gluck and coworkers used sphingomyelin as an internal
standard and compared the amount of lecithin with that of
sphingomyelin.
 Amniotic fluid sphingomyelin exceeds lecithin until 31 to 32
weeks, when the L/S ratio reaches 1.
 Lecithin then rises rapidly, and an L/S ratio of 2.0 is
observed at approximately 35 weeks. Wide variation in the
L/S ratio at each gestational age has been noted.
 Nevertheless, a ratio of 2.0 or greater has repeatedly been
associated with pulmonary maturity

23. PG, which does not appear until 35 weeks' gestation and
increases rapidly between 37 to 40 weeks, is a marker
of completed pulmonary maturation
 Most infants who lack PG but who have a mature L/S
ratio fail to develop RDS. However, PG may provide
further insurance against the onset of RDS despite
intrapartum complications.
 This assay can detect PG at a concentration greater than
0.5 mg/ml of amniotic fluid.
 The test takes 20 to 30 minutes to perform and
requires only 1.5 ml of amniotic fluid.
 Besides being highly sensitive, several studies have
found a positive Amniostat-FLM to correlate well with
the presence of PG by thin-layer chromatography and
the absence of subsequent RDS.

24.  TDx Test (Surfactant Albumin Ratio)
 The TDx analyzer, an automated fluorescence
polarimeter, has been used to assess surfactant
content in amniotic fluid.
 The test requires 1 ml of amniotic fluid and can be
run in less than 1 hour. The surfactant albumin ratio
(SAR) is determined with amniotic fluid albumin used
as an internal reference.
 A value of 70 was considered mature with the original
assay, whereas with the newer FLM-II test, 55 is the
mature cut-off.[215]
 A mature value reliably predicts the absence of RDS
requiring intubation in infants of diabetic mothers.

25.  Foam Stability Index
 The test is based on the manual foam stability index (FSI), and
is a variation of the shake test.[243]
 The kit currently available contains test wells with a
predispensed volume of ethanol.
 The addition of 0.5-ml amniotic fluid to each test well in the
kit produces final ethanol volumes of 44 to 50 percent. A
control well contains sufficient surfactant in 50-percent
ethanol to produce an example of the stable foam end point.
 The amniotic fluid/ethanol mixture is first shaken, and the FSI
value is read as the highest value well in which a ring of stable
foam persists.[244]
 This test appears to be a reliable predictor of fetal lung
maturity.[245] Subsequent RDS is very unlikely with an FSI value
of 47 or higher.
 The methodology is simple, and the test can be performed at
any time of day by persons who have had only minimal
instruction

26. Visual Inspection
 During the first and second trimesters, amniotic fluid is yellow and clear. It
becomes colorless in the third trimester.
 By 33 to 34 weeks' gestation, cloudiness and flocculation are noted, and, as
term approaches, vernix appears.
 Amniotic fluid with obvious vernix or fluid so turbid it does not permit the
reading of newsprint through it will usually have a mature L/S ratio.[246]
Lamellar Body Counts
 Lamellar bodies are the storage form of surfactant released by fetal type II
pneumocytes into the amniotic fluid. Because they have the same size as
platelets, the amniotic fluid concentration of lamellar bodies may be determined
using a commercial cell counter.
 The test requires less than 1 ml of amniotic fluid and takes only 15 minutes to
perform. A lamellar body count greater than 30,000 to 55,000/ml is highly
predictive of pulmonary maturity, whereas a count below 10,000/ml suggests a
significant risk for RDS.
 The ease and relatively low cost of this test has contributed to its popularity,
although poor concordance among various instruments for the assay of lamellar
body counts has been noted.[252]

27.  A large number of techniques are now available to assess
fetal pulmonary maturation.
 Several rapid screening tests, including the TDx test and
lamellar body count, appear to be highly reliable when
mature. In an uncomplicated pregnancy, when a screening
test such as the TDx demonstrates fetal pulmonary
maturation, one can safely proceed with delivery.
 The more complicated, expensive, and timely L/S ratio may
be reserved for those borderline TDx or lamellar body count
results in the clinical circumstance of a fetus that may
benefit from delivery if maturity is ultimately confirmed with
advanced testing.
 This sequential approach is also extremely cost effective.
 When the screening test is immature, the L/S ratio and PG
assessment should be considered.

28.  women w/ high risk-factors for stillbirth should
have surveillance
 -start testing 32-34 wks for most, 26-28 if mult
risk
 testing weekly or twice weekly depending on
severity
 -any sig deterioration in maternal status or fetal
activity warrants further eval regardless of time
elapsed
 -oligo requires del in term and close monitoring in
preterm
 In absence of contraindication may attem induction
in fetus w/ abnl test results
 -MCA dopplers considered investigational in

30.  The goals of intrapartum fetal evaluation by EFM and available back-up methods
are to detect fetal hypoxia, reverse the hypoxia with nonsurgical means, or if
unsuccessful, determine if the hypoxia has progressed to metabolic acidosis, and if
so, deliver the baby expeditiously to avoid the hypoxia and acidosis from resulting
in any damage to the baby.
□ EFM is an inherently suboptimal method of determining fetal hypoxia and
acidosis, because many factors besides these variables may alter the FHR and
mimic changes caused by hypoxia and acidosis. When the FHR is normal, its
reliability in predicting the absence of fetal compromise is high, but when the
FHR is abnormal, its reliability in predicting the presence of asphyxia is poor.
□ The term fetal distress should be abandoned in favor of nonreassuring fetal status,
because when the fetal monitor suggests that there may be a problem, in most
circumstances, we can only say that we are no longer reassured with a high degree
of certainty that the fetus is well oxygenated.
□ Late decelerations are always indicative of relative fetal hypoxia, and are caused by
inadequate oxygen delivery, exchange, or uptake that is aggravated by the
additional hypoperfusion of the placenta caused by contractions.
Variable decelerations are caused by a decrease in umbilical cord flow resulting from
cord compression or cord stretch.
Prolonged decelerations may be caused by any mechanism that decreases fetal
oxygenation.

31. □ In labor, loss of variability, loss of accelerations, and tachycardia
should be interpreted only as indicative of fetal compromise in
the presence of nonreassuring decelerations (late, nonreassuring
variable or prolonged decelerations), as signs of hypoxia should
always precede signs of neurologic depression secondary to
hypoxia.
□ In the presence of oligohydramnios and variable decelerations,
or with meconium, intrapartum amnioinfusion has been shown
to decrease rates of cesarean delivery for NRFS and may
decrease neonatal respiratory complications caused by
meconium aspiration.
□ In the presence of an otherwise nonreassuring FHR pattern, the
presence of accelerations of the FHR, either spontaneous or
elicited by scalp stimulation or vibroacoustic stimulation,
indicate the absence of fetal acidosis. Their absence is
associated with a 50 percent chance of fetal acidosis, but only in
the setting of a nonreassuring FHR.
□ Umbilical cord blood gases should be obtained and documented
in situations in which there is a nonreassuring or confusing FHR
pattern during labor, there is neonatal depression following
birth, with premature babies, and when suctioning for meconium
is performed. These values will help clarify the reasons for
abnormal FHR patterns or for neonatal depression

32. □ Fetal pulse oximetry was approved in May 2000 by the Food and
Drug Administration for use in term (≤ 36 weeks) patients with
nonreassuring FHR patterns. This technology may improve our
ability to more accurately interpret nonreassuring FHR patterns
and may have the potential to decrease cesarean deliveries for
NRFS.
□ Although there is correlation between a nonreassuring FHR
pattern and neonatal depression, the FHR is a poor predictor of
long-term neurologic sequelae. Furthermore, fetuses with
previous neurologic insults may have significantly abnormal FHR
patterns, even when they are well oxygenated in labor.
The purpose of FHR monitoring is to detect fetal hypoxia and
metabolic acidosis. Many fetuses develop hypoxia intermittently
but never progress to metabolic acidosis.
The ideal is to avoid intervention for hypoxia, but to intervene in
the presence of early metabolic acidosis before it can result in
tissue damage or fetal death.

33.  Criteria for fetal distress that were to remain
essentially unchanged until the arrival of
electronic FHR monitoring.
 These included
◦ Tachycardia (FHR > 160 beats per minute [bpm]),
◦ Bradycardia (FHR < 100 bpm),
◦ Irregular heart rate,
◦ Passage of meconium, and
◦ Gross alteration of fetal movement

34.  Doppler became the dominant modality for external
monitoring.
 Ultimately, better Doppler devices coupled with
autocorrelation formulas for processing the signal
have resulted in excellent external FHR signals that
can be relied upon clinically.
 External monitoring is necessary at all times when
the membranes are intact and cannot or should not
be ruptured.
 In addition, certain clinical situations make it unwise
to puncture the skin with a fetal electrode for fear of
vertical transmission of infection to the fetus. Such
conditions include maternal infection with human
immunodeficiency virus (HIV), hepatitis C, and
herpes simplex.

35.  Contractions are detected by the pressure-sensitive
tocodynamometer, amplified, and then recorded. Fetal
heart rate is monitored using the Doppler ultrasound
transducer, which both emits and receives the reflected
ultrasound signal that is then counted and recorded.
 The external monitoring device, or tocodynamometer, is
basically a ring-style pressure transducer attached to the
maternal abdomen via a belt that maintains tight
continuous contact.
 When the uterus contracts, the change in its shape and
rigidity depresses the plunger of the sensor, which
changes the voltage of the electrical current.
 The change in voltage is proportional to the strength of
the uterine contractions. The tocodynamometer depicts
the frequency of the contractions accurately, but the
strength of the contractions only relatively, becaise it
cannot measure actual intrauterine pressure

36.  The advantage of the external monitor is that
it can be used when membranes are intact
and it is noninvasive.
 Its disadvantages, in addition to its inherently
limited accuracy, is that it is more
uncomfortable for the mother and limits her
mobility.
 Contractions can be more accurately
monitored through an intrauterine pressure
catheter

37.  It is often necessary to apply an internal
electrode to obtain a high-quality, accurate,
continuous FHR tracing.
 This is especially true in patients who are obese,
those with a premature fetus, or when the
mother or fetus is moving too much to obtain an
adequate signal.
 The original internal electrode was made from a
modified skin clip that required a special
instrument to place it on the fetal scalp
 The FHR tracing results from the signal
processor, which counts every R-R interval of
the ECG from the scalp electrode, converts this
interval to rate, and displays every interval (in
rate as beats per minute) on the top channel of
the two-channel fetal monitor recording pape

38.  Uterine contractions are assessed with an intrauterine
pressure catheter connected to a pressure
transducer. This signal is then amplified and
recorded.
 The fetal electrocardiogram is obtained by direct
application of the scalp electrode, which is then
attached to a leg plate on the mother's thigh. The
signal is transmitted to the monitor, where it is
amplified, counted by the cardiotachometer, and then
recorded.
 This is a tracing from an internal electrode
demonstrating an apparent bradycardia with a rate of
about 90 bpm.
 In actuality, this tracing is from a dead fetus, and the
automatic gain amplifier increases the amplitude of
the maternal ECG signal, allowing the monitor to
count and display the maternal heart rate

39.  The goal of monitoring is to maintain adequate,
high-quality, continuous FHR and contraction
tracings while maintaining maximum maternal
comfort and avoiding the risk of trauma or infection
to the fetus and mother.
 External devices minimize risk but often give less
accurate information and are more uncomfortable for
the mother.
 In general, when the FHR is reassuring and there is an
adequate tracing and when the progress of labor is
adequate, the external devices are fine.
 When a better quality FHR tracing is required or it
becomes important to accurately assess uterine
contraction duration and intensity, then internal
devices may be necessary.

40.  The basis of FHR monitoring is, in a real sense,
fetal brain monitoring.
 The fetal brain is constantly responding to
stimuli, both peripheral and central, with signals
to the fetal heart that alter the heart rate on a
moment-to-moment basis.
 Such stimuli to which the brain responds include
chemoreceptors, baroreceptors, and direct
effects of metabolic changes within the brain
itself

41.  The FHR has many characteristics that we are
able to use to accomplish this interpretation.
These include the baseline rate; the variability
of the FHR from beat to beat; transient
alterations below the baseline, termed
decelerations; and transient alterations above
the baseline, termed accelerations.
 Rate and variability are generally included as
characteristics of the baseline FHR, and
decelerations and accelerations as periodic
changes.*

42.  The baseline FHR is typically between 120 and
160 bpm.
 In very early gestation (15 to 20 weeks), the FHR
is significantly higher than in the term fetus.
 The decline in FHR represents a maturation of
fetal vagal tone with progressing gestation.
 Thus, the baseline heart rate is largely a
function of vagal activity
 Rates above 160 bpm are called tachycardia.
Tachycardia may have great clinical significance.

43.  The two most common causes of tachycardia are
maternal fever and drugs that directly raise the
fetal heart rate.
 Maternal fever raises the core temperature of
the fetus, which is always about 1°F higher than
the maternal temperature.
 With maternal fever, virtually all fetuses have
tachycardia .
 The FHR rises approximately 10 bpm for each
1°F increase in maternal temperature. Because at
term with chorioamnionitis only 1 to 2 % of
fetuses are septic, the tachycardia is unlikely to
indicate fetal sepsis but rather is probably
caused by an increase in fetal metabolic rate
associated with the elevated temperature.

44.  Drugs that elevate the FHR fall into one of two
categories: vagolytic and b-sympathomimetic.
 Vagolytic include scopalomine, atropine and
phenothiazines, and hydroxyzine.
 These drugs, however, rarely raise the FHR above
160 bpm. b-Sympathomimetics include
terbutaline and ritodrine, used for preterm labor,
and terbutaline and epinephrine, used for
bronchospasm
 Other less common causes of fetal tachycardia
include fetal hyperthyroidism, fetal anemia, fetal
heart failure, and fetal tachyarrhythmias.

45.  An FHR less than 120 bpm is termed a
bradycardia
 A prolonged deceleration to less than 120 bpm
lasting more than 60 to 90 seconds may often
indicate significant fetal hypoxia .
 True fetal bradycardias are due to several possible
causes. In the range of 90 to 120 bpm, a
bradycardia may often be a normal variant, and
these fetuses are usually bradycardic after birth
but are otherwise well oxygenated and norma. As
with tachycardia and fever, maternal hypothermia
may cause fetal bradycardia.
 A number of drugs may also result in fetal
bradycardia.

46.  A fetal baseline heart rate in the range of 80 bpm or less,
especially with reduced variability, may be caused by a
complete heart block.
 Complete heart block may result from antibodies
associated with maternal lupus erythematosus, may be
seen with congenital cardiac anomalies, or is idiopathic.
 Although a heart block is not associated with hypoxia, it
makes the FHR essentially useless in monitoring fetal
oxygenation, because the fetal brain is no longer
communicating with the ventricle of the heart that is being
monitored.
 Finally, when a patient is admitted with a baseline
bradycardia, one should also consider the possibility of
maternal heart rate being recorded with a dead fetus
(whether internal or external monitor).
 Real-time ultrasound is used to verify that the bradycardia
is fetal in origin.

47.  Differences in heart rate from beat to beat are
recorded as variability reflected visually as a line that
fluctuates above and below the baseline.
 This variability is a reflection of neuromodulation of
the FHR by an intact and active CNS and also reflects
normal cardiac responsiveness
 Short-term variability is the beat-to-beat irregularity
in the FHR and is caused by the difference in rates
between successive beats of the FHR. It is caused by the
push-pull effect of sympathetic and parasympathetic
nerve input, but the vagus nerve has the dominant role in
affecting variability
 Long-term variability is the waviness of the FHR tracing,
and is generally seen in three to five cycles per minute
 No clear evidence that distinguishing between the two is
helpful clinically.

48.  When the fetus is alert and active, the FHR variability is normal
or increased.
 When the fetus is obtunded, owing to whatever cause, the
variability is reduced.
 Because severe hypoxia, especially when it reaches the level
of metabolic acidosis, always depresses the CNS,
 Unfortunately, the converse is not true, because there are
many factors that cause the CNS to be depressed
 Normal variability reliably indicates the absence of severe
hypoxia and acidosis .

49.  In general, anything that is associated with
depressed or reduced brain function will diminish
variability. These include ;
o fetal sleep cycles;
◦ drugs, especially CNS depressants;
◦ fetal anomalies, especially of the CNS; and
◦ previous insults that have damaged the fetal brain.
 FHR variability is also affected by gestational age,
and very immature fetuses of less than 26 weeks'
gestation often have reduced variability from an
immature CNS.
 In addition, as heart rate increases with fetal
tachycardia, variability is often reduced from the
rate alone, as sympathetic dominance overrides the
natural influence of the vagus.

50.  Variability, tachycardia, and bradycardia are
characteristic alterations of the baseline heart
rate.
 Periodic changes of the FHR include
decelerations and accelerations.
 These are transient changes in the fetal heart
rate of relatively brief duration, with return to
the original baseline FHR.
 In labor, these changes usually occur in response
to uterine contractions but may also occur with
fetal movement.

51.  There are four principal types of
decelerations: early, late, variable, and
prolonged.
 These are named for their timing, relationship
to contractions, duration, and shape, but they
are important distinctions more because they
describe the cause of the decelerations

52. Early decelerations are shallow, symmetric, uniform
decelerations with onset and return that are gradual,
resulting in a U-shaped deceleration.
They begin early in the contraction, have their nadir
coincident with the peak of the contraction, and
return to the baseline by the time the contraction is
over
Early decelerations are not associated with
accelerations that precede or follow the deceleration.
These decelerations rarely descend more than 30 to 40
bpm below the baseline rate.
They are thought to be caused by compression of the
fetal head by the uterine cervix as it overrides the
anterior fontanel of the cranium.
This results in altered cerebral blood flow, precipitating
a vagal reflex with the resultant slowing of the FHR.

53.  Because the cervix creates the pressure, these
decelerations are usually seen between 4 and
6 cm of dilation
 They do not indicate fetal hypoxia and are
only significant in that they may be easily
confused with late decelerations because of
their similar shape and depth.
 They are the most infrequent of decelerations,
occurring in about 5 to 10 percent of all
fetuses in labor.

55.  Late decelerations are similar in appearance to early decelerations.
 They, too, are of gradual onset and return, U-shaped, and generally
descend below the baseline no more than 30 to 40 bpm, although there
are exceptions.
 However, in contrast to early decelerations, late decelerations are
delayed in timing relative to the contraction.
 They begin usually about 30 seconds after the onset of the contraction
or even at or after its peak.
 Their nadir is after the peak of the contraction.
 FHR variability may be unchanged or even increased during the
decelerations.
 These decelerations are not associated with accelerations immediately
preceding or following their onset and return
 Late decelerations are generally said to be caused by uteroplacental
insufficiency.
 This implies that uteroplacental perfusion is temporarily interrupted
during the peak of strong contractions.
 The fetus that normally will not become hypoxic with this temporary halt
in blood flow may do so if there is insufficient perfusion or oxygen
exchange at other times

56.  Oxygen within the fetal brain detect a relative drop in fetal
oxygen tension ---- increase in sympathetic neuronal
response ---- elevation in fetal blood pressure ------( when
detected by baroreceptors), produces a protective slowing in
the FHR in response to the increase in peripheral vascular
resistance.
 This has been referred to as the reflex type of late
deceleration. This complex double reflex is probably the
reason the deceleration is delayed.
 During this type of reflex, the depth of the deceleration is
proportional to the severity of the hypoxia and the
deceleration moves closer to the contraction as the hypoxia
becomes more severe.
 However, there is also a second type of late deceleration,
caused by myocardial depression. As the hypoxia continues
and becomes more severe, late decelerations are no longer
vagally mediated and are seen even with interruption of the
vagus nerve; thus, they are directly myocardial in origin.
 These decelerations are not proportional in their depth to the
severity of the hypoxia, and actually may become more
shallow as the hypoxia becomes severe
 Generally agreed that the depth of the late deceleration
cannot be used to judge the severity of the hypoxia

57.  Because of the mechanisms causing these changes, late decelerations
always indicate fetal hypoxia.
 Only the severity of the hypoxia and the overall duration of the late
decelerations will determine whether a metabolic acidosis will occur, and
this is highly unpredictable(relative drop from baseline oxygenation
rather than an absolute number)
 Thus, the fetus accustomed to higher than average oxygen saturation
may have a drop in oxygen at or only slightly below the normal range; a
level deep enough to signal a late deceleration but not low enough to
require anaerobic metabolism.
 Another important point in understanding the results of hypoxia
associated with late decelerations is that the placenta's capacity for
exchanging oxygen is substantially less than its capacity for exchanging
carbon dioxide.
 In situations in which there are persistent late decelerations and the fetus
becomes sufficiently hypoxic to develop a metabolic acidosis, there may
be no retention of carbon dioxide.
 This is analogous to the adult with lung disease but no airway disease in
whom hypoxia is often seen without difficulty in eliminating CO2.
 Thus, the metabolic acidosis is usually not mixed with a respiratory
acidosis. The only common exception to this is with abruptio placentae,
in which CO2 retention is seen with late decelerations.

58.  Causes of late decelerations include any
factor that can alter delivery, exchange, or
uptake of oxygen at the fetal-maternal
interface within the placenta.
 Conduction anesthesia (spinal or epidural)
can cause either systemic or local
hypoperfusion/hypotension, and thus the
level of contractions required to interrupt
uterine blood flow is lower, and again the
duration of interruption of uterine blood flow
is prolonged

59.  The most common pathologic conditions of the
placenta associated with late decelerations are
either microvascular disease in the placenta or
local vasospasm compromising blood flow and
thus exchange.
 Common causes include
o Postmaturity,
o Maternal hypertension (chronic hypertension or preeclampsia),
o Collagen vascular diseases, and
o Diabetes mellitus in its more advanced stages.
o Abruptio placentae
o Maternal anemia or maternal hypoxemia
o Chronic fetal anemia may diminish

60.  The most common type of decelerations seen in the
laboring patient is variable decelerations.
 Variable decelerations are, in general, synonymous
with umbilical cord compression, and anything that
results in the interruption of blood flow within the
umbilical cord will result in a variable deceleration.
 The variable deceleration is the most difficult pattern
to describe verbally, but the easiest to recognize
visually.
 First and foremost, the term variable is by far the
best single word to describe this type of
deceleration.
 They are variable in all ways: size, shape, depth,
duration, and timing relative to the contraction.
 The onset is usually abrupt and sharp. The return is
similarly abrupt in most situations.

61.  The depth and duration are proportional to the
severity and duration of interruption of cord blood
flow.
 Variable decelerations are usually seen with
accelerations immediately preceding the onset of the
deceleration and immediately following the return to
baseline.
 The NICHD Research Planning Workshop proposed that
the duration of a variable deceleration should be
limited to 2 minutes, and that beyond 2 minutes, it
should be called a prolonged deceleration.
 However, most definitions in the past have not put a
limit on duration but rely more on the appearance of
the deceleration.

62.  When the umbilical cord is compressed ----
decreased cardiac return, fetal hypotension( a
baroreceptor reflex ) ----- accelerate the heart
rate (brain ) ---- With continuing compression ---
-the fetus detects an increase in systemic vascular
resistance ---- baroreceptors detect the increase
in resistance, and the heart slows as a protective
mechanism.
 This increase in heart rate is the acceleration that
precedes the variable deceleration
 This is probably the reason that with variable
decelerations, any combination of deceleration
with acceleration preceding, preceding and
following, following only, neither, or even
acceleration alone may be seen with cord
compression,

63.  Variable decelerations are seen in the vast
majority of all labors, and most often, these
decelerations occur without fetal hypoxemia.
Mild
 Deceleration of a duration of <30 seconds,
regardless of depth
 Decelerations not below 80 bpm, regardless of
duration
Moderate
 Deceleration with a level <80 bpm
Severe
 Deceleration to a level <70 bpm for >60 seconds

64.  There are four categories of causes of cord
compression patterns that are useful to consider
from a management standpoint.
 Variable decelerations appearing early in labor are
often caused by oligohydramnios.
 Nuchal cords, wherein the cord becomes stretched
with descent of the fetal head, and as previously
described, cord stretch is a profound stimulus for
vasospasm in the cord vessels (8 to 9 cm of dilation).
 Unusual types of abnormal umbilical cords, such as
short cords, true knots, velamentous cord insertion,
cord looped around the extremities, occult cord
prolapse, and velamentous insertion of the cord will
produce unpredictable onsets in the timing of the
appearance of variable decelerations. And
 Finally, the rarest form of cord compression, and one
that usually requires rapid delivery by cesarean
section, is true umbilical cord prolapse.

65.  Because the umbilical cord is most analogous to the
adult trachea, interruption in cord flow results in both
retention of CO2 and cessation of O2 delivery.
 When this becomes progressive, the intermittent
compression often first leads to a progressive
increase in fetal CO2, which results in a respiratory
acidosis.
 If the cord compression continues and also is
sufficiently severe to cause insufficient delivery of
oxygen, then a metabolic acidosis can also develop.
 Thus, in a fetal acidosis resulting from cord
compression, the acidosis can be respiratory or
combined respiratory and metabolic but should not
be metabolic

66.  Prolonged decelerations are isolated decelerations lasting
90 to 120 seconds or more.
 The NICHD Research Planning Workshop proposed that
prolonged decelerations be defined as those lasting 2 to 10
minutes, and that beyond 10 minutes, it is a baseline
change.
◦ Although this proposal is meant to create uniform definitions, it
belies the pathophysiology of the deceleration, because the sudden
drop in FHR is the result of some adverse afferent stimulus and if
sustained will result in a prolonged decrease in FHR.
◦ Thus, this is not really a baseline change, because the FHR will
return to or near its original baseline when the stimulus is removed.
 Prolonged decelerations may be caused by virtually any of
the mechanisms previously described, but usually are of a
more profound and sustained nature.
 Prolonged umbilical cord compression, profound placental
insufficiency, or possibly even sustained head compression
may lead to prolonged decelerations.

67.  The presence of and severity of hypoxia are thought
to correlate with the following variables with a
prolonged deceleration
 Examples of this type of deceleration include a
o prolapsed umbilical cord or other forms of prolonged cord
compression,
o prolonged uterine hyperstimulation,
o hypotension following conduction anesthesia,
o severe degrees of abruptio placentae,
o paracervical anesthesia,
o an eclamptic seizure, and
o rapid descent through the birth canal.
 Occasionally, less severe stimuli such as
o examination of the fetal head,
o Valsalva's maneuvers, or
o application of a scalp electrode may cause milder forms of
prolonged decelerations.

68.  Accelerations are periodic changes of the FHR above the baseline .
They are not classified by type.
 Except for those accelerations previously described that are
associated with variable decelerations, virtually all accelerations
are a physiologic response to fetal movement.
 Accelerations are usually short in duration, lasting no more than
30 to 90 seconds, but in an unusually active fetus, they can be
sustained as long as 30 minutes or more.
 Again, the NICHD Research Planning Workshop disagrees
somewhat on this definition. They propose that accelerations of
more than 10 minutes be defined as a change in baseline.
 However, sustained accelerations are associated with an actively
moving fetus, and when the fetus becomes quiet, the FHR will
return to baseline.
 It is important that these accelerations not be confused with a
baseline change, because sustained accelerations, which are
consistent with a well-oxygenated, vigorous fetus, can be
confused visually with fetal tachycardia, and the return of the FHR
to the original baseline can be confused with decelerations.

69.  The absence of accelerations means only that the baby is not
moving.
 Because accelerations can be quantified in beats per minute above
the baseline and duration, their presence is less subjective than
quantifying FHR variability
 The 15 bpm above the baseline lasting for more than 15 seconds
 Earlier in gestation, accelerations are less frequent and of lower
amplitude. Fetuses of younger than 32 weeks have been defined as
having accelerations if they exceed 10 bpm for more than 10
seconds.
 If there is no acceleration in the face of an otherwise nonreassuring
FHR, most studies have shown that about 50 percent of these fetuses
have an acidotic pH value on scalp sampling.
 However, the absence of accelerations in a fetus without a
nonreassuring deceleration pattern rarely indicates fetal acidosis.

70.  This pattern is strongly associated with fetal hypoxia,
most often seen in the presence of severe fetal anemia.
 Using strict criteria for this pattern, there will be a high
correlation with significant fetal acidosis or severe
anemia.
 These criteria for identifying a sinusoidal FHR include
◦ (1) a stable baseline FHR of 120 to 160 bpm with regular sine
wavelike oscillations,
◦ (2) an amplitude of 5 to 15 bpm,
◦ (3) a frequency of 2 to 5 cycles/min,
◦ (4) fixed or absent short-term variability,
◦ (5) oscillation of the sine wave above and below the baseline,
and (6) absence of accelerations.
 There are relatively commonly seen FHR patterns that
mimic sinusoidal patterns (pseudosinusoidal) that are
associated with well-oxygenated and nonanemic
fetuses.

71.  Oxygen Administration (5ml/10ml via int
nasal/mask)
 Lateral Positioning
 Hydration
 Oxytocin-D/C
 Tocolytics
 Amnioinfusion (1000ml N/S –decrease MAS &
impruve APGAR score)