1. Management of Intrapartum
Fetal Heart Rate Tracings
ACOG
Number 116, November 2010

2. DO NOT INTERPRET FHR in ISOLATION
• TIMING IS IMPORTANT ie MULTIP MOVING QUICKLY vs NULLIP
with unfavorable cervix OR IN EARLY LABOR or INDUCTION
• PELVIS & BABY SIZE & OB HISTORY & OB Complications
• CLINICAL FACTORS
– Gestational age ( Postdates / < 32 weeks )
– Maternal Medical Complications ( ?Exacerbation?)
– Previous Fetal Status (Change from admission?)
– Fetal Complications (IUGR, Oligohydramnios, Anomalies, Abruption,
Postdates)
– Medications ( Narcotics, B sympatho, Ephedrine, B blockers,)
MISCELLANEOUS FACTORS
– Fever, Meconium, Magnesium Sulfate, Epidural, Vaginal bleeding,
VABC, Recent AROM, Smoking , illicit drugs

3. Physiologic Control of FHR
• Normal FHR patterns rely on sympathetic
and parasympathetic activity AND ability
of the heart to respond appropriately to
the input from the nervous system
• Parasympathetic and Sympathetic nervous
system are dependent on intact functioning
CNS with no preceding damage or
significant anatomical anomaly or insult
• Normal function of CNS & Myocardium both
depend on adequate oxygenation

4. T 18 WITH CNS ANOMALY

5. VARIABILITY INFLUENCED BY

6. VARIABILITY INFLUENCED BY

7. Physiologic Control of FHR
• Sinoatrial node (fastest rate)
• Atrial node (next fastest)
• Ventricular rate (slowest 60 bpm or less)
• Sympathetic nervous system (increases
heart rate)
• Parasympathetic nervous system
(decreases heart rate)

8. PHYSILOGY EARLY Decelerations
• Early decelerations caused by
– Vagal stimulation commonly associated with
Head compression / Prolonged vaginal exam
– Results in a normal physiologic decrease in
fetal heart rate not associated with fetal
hypoxemia or acidosis

9. PHYSILOGY EARLY Decelerations

10. Physiology of VARIABLE Decelerations
• Variable deceleration
– Cord compression leads to increased venous
pressure.
– Pressure sensed in baroreceptors resulting in
Vagal nerve stimulation
– Vagal nerve stimulation results in decreased
fetal heart rate

11. Physiology of VARIABLE Decelerations

12. PHYSIOLOGY LATE Decelerations
• Late deceleration
– Reflex
• Decrease in blood flow delivered to the baby ( maternal
hypotension/maternal venous compression/cord
compression/occlusion/uterine hyperstimulation) resulting in
the inability to deliver enough O2 to the baby
• OR deoxygenated blood delivered to the baby (
abruption/maternal seizure/ ss crisis/pneumonia/PE/asthma)
resulting in low PaO2 sensed by chemoreceptors which
results in vagal discharge resulting in slowing of heart rate
– Non-reflex
• Deoxygenated blood insufficient to support normal
myocardial contarctions resulting in direct myocardial
depression

13. PHYSIOLOGY LATE Decelerations

14. NICHD NOMENCLATURE
STANADARDIZED NOMENCLATURE
should lead to comparable research & improved
communication
• Revised and Presented in 2008 by NICHD
• NICHD nomenclature endorsed by
– American College of Obstetricians and Gynecologists
– American Women’s Health, Obstetric, and Neonatal
Nursing

15. NICHD NOMENCLATURE
• Baseline
• Periodic
– Associated with uterine contractions
– Distinguished on basis of onset of waveform
• Abrupt
• Gradual
• Episodic
– Not associated with uterine contractions

16. NICHD NOMENCLATURE
• No distinction made between short-term
variability and long-term variability
• Variability defined visually based on
amplitude of FHR complexes

17. SHORT & LONG TERM
VARIABILITY

18. NICHD NOMENCLATURE
• Full description of FHR tracing requires:
– Contraction pattern
– Fetal heart rate
– Variability
– Accelerations
– Periodic or Episodic Decelerations
– Changes or trends of FHR patterns over time

19. Uterine Contractions
• Number of contractions in 10-minute
window, averaged over 30 minutes
Tachysystole
> 5 contractions in 10 minutes

20. Uterine Contraction Descriptions
• Tachysystole qualified as to
presence/absence of decelerations
• Tachysystole applies to spontaneous or
stimulated labor
• Terms hyperstimulation and
hypercontractility are not defined and
should be abandoned

21. CATEGORY II OR III
TACHYSYSTOLE
GOAL REDUCE UTERINE ACTIVITY
• Discontinue oxytocin or cervical ripening
agents
• Administer tocolytic medication
( Brethine 0.25 mg SQ only if necessary )
• DO NOT USE BRETHINE FOR TACHYSYSTOLE
ASSOCIATED ABRUPTION

22. MANAGEMENT OF TACHYSYSTOLE

23. NICHD NOMENCLATURE
BASELINE FETAL HEART RATE
The mean FHR rounded to increments of 5 beats per minute during a
MINIMUM OF 2 MINUTES AND < 1O MINUTES EXCLUDING :
—Periodic or episodic changes
— Periods of marked FHR variability
— Segments of baseline that differ by more than 25 beats per minute
•The baseline must be for a minimum of 2 minutes in any 10-
minute segment, or the baseline for that time period is indeterminate. In
this case, one may refer to the prior 10-minute window for determination of
baseline.
• Normal FHR baseline: 110–160 beats per minute
• Tachycardia: FHR baseline is greater than 160 beats per minute
• Bradycardia: FHR baseline is less than 110 beats per minute

24. NICHD NOMENCLATURE
BASELINE VARIABILITY
Fluctuations in the baseline FHR that are irregular in
amplitude and frequency. Variability is visually
quantitated as the amplitude of peak-to-trough in beats
per minute.
• Absent — amplitude range undetectable
• Minimal —amplitude range detectable but 5 beats per
minute or fewer
• Moderate (normal)—amplitude range 6–25 beats per
minute
• Marked —amplitude range greater than 25 beats per
minute

25. Variability
Amplitude range Descriptive term
Undetectable Absent
< 5 bpm Minimal
6-25 bpm Moderate
> 25 bpm Marked

26. Absent
Minimal
Moderate
Marked
Sinusoidal

27. NICHD NOMENCLATURE
ACCELERATION
• A visually apparent abrupt increase (onset to peak in less than 30 seconds)
in the FHR above the baseline
• At 32 weeks of gestation and beyond, an acceleration has a peak of 15
beats per minute or more above baseline, with a duration of 15 seconds
or more but less than 2 minutes from onset to return.
• Before 32 weeks of gestation, an acceleration has a peak of 10 beats per
minute or more above baseline, with a duration of 10 seconds or more but
less than 2 minutes from onset to return.
• Prolonged ACCELERATION
> 2 minutes < 10 minutes in duration
BASELINE CHANGE
If an acceleration lasts >/= to 10 minutes
it is a baseline change

28. LATE DECELERATIONS
• Late deceleration
– Visually apparent gradual (defined as onset of
deceleration to nadir ≥30 seconds) decrease and
return to baseline FHR associated with uterine
contraction
– The decrease calculated from most recent portion of
baseline
– The deceleration is delayed in timing, with the nadir
of the deceleration occurring after the peak of the
contraction.
• In most cases the onset, nadir, and recovery of
the deceleration occur after the beginning, peak,
and ending of the contraction, respectively

29. LATE DECLERATIONS

30. EARLY DECELERATIONS
• Early deceleration
– Visually apparent gradual decrease (defined as onset
of deceleration to nadir ≥30 seconds) and return to
baseline FHR associated with uterine contraction
– Calculated from most recent portion of baseline
– Coincident in timing, with nadir of deceleration
occurring at same time as the peak of contraction
• In most cases onset, nadir, and recovery of
deceleration are coincident with the beginning,
peak, and ending of the contraction, respectively

31. VARIABLE DECELERATIONS
• Variable deceleration
– Visually apparent abrupt decrease (defined as onset
of deceleration to beginning of nadir <30 seconds) in
FHR below the baseline
– The decrease is calculated from most recent portion
of baseline
– The decrease in FHR below baseline is ≥15
beats/min, lasting ≥15 seconds, and <2 minutes from
onset to return to baseline.
• When variable decelerations are associated with
uterine contractions, their onset, depth, and
duration commonly vary with successive uterine
contractions

32. PROLONGED DECELERATION
>/= 2 & < 10 minutes
– Decrease in FHR below baseline calculated
from most recent10 minute stable baseline
– Decrease from baseline is ≥15 beats/min,
lasting ≥2 minutes, but <10 minutes from
onset to return to baseline.
• IF 15 BPM DECELERATION LAST
≥ 10 minutes it is a
FETAL HEART RATE BASELINE CHANGE

33. QUANTIFICATION OF
DELERATIONS & ACCELERATIONS
• Decelerations are quantitated by the depth of the nadir in
BPM below baseline
• The duration is quantitated in minutes and seconds from
beginning to end of deceleration
• Accelerations are quantitated similarly
• Decelerations may be defined as recurrent if they occur
with ≥50% of uterine contractions in any 20-minute
segment
• Bradycardia and tachycardia are quantitated by actual
FHR in BPM.

34. Interpretation of FHR patterns
• New three-tier system
• FHR tracing patterns reflect current fetal
acid-base status
• FHR tracing patterns cannot RELIABLY
OR CONSISTENTLY predict development
of cerebral palsy

35. Category I
Category I FHR tracings include all of the following:
• Baseline rate:110–160 beats per minute
• Baseline FHR variability: MODERATE
• Late or Variable Decelerations
ABSENT
• Early decelerations: May be present
• Accelerations: Present or ABSENT

36. Category I FHR tracing
• Includes ALL of the following:
– Baseline rate NORMAL : 110-160 BPM
– Baseline Variability: MODERATE
– Late or Variable Decelerations: ABSENT
– Early Decelerations: PRESENT OR ABSENT
– Accelerations: PRESENT OR ABSENT
• Category I FHR tracings are normal
– Strongly predictive of normal fetal acid-base status at
time of observation
- Requires no change in management

37. Category II FHR tracing
Includes ANY of the following
RATE
1) Bradycardia not accompanied by absent baseline
variability
2) Tachycardia
Baseline FHR variability
1) Minimal baseline variability
2) Absent baseline variability with no recurrent
decelerations
3) Marked baseline variability

38. Category II FHR tracing
ACCELERATIONS
– Absence of induced accelerations after fetal
stimulation
–NO FETAL HEART RATE
ACCELERATIONS WITH FAS
OR SCALP STIMULATION

39. Category II FHR tracing
PERIODIC OR EPISODIC DECELERATIONS
• Recurrent variable decelerations accompanied by
minimal or moderate baseline variability
• Prolonged deceleration more than 2 minutes but
less than10 minutes
• Recurrent late decelerations with moderate baseline
variability
• Variable decelerations with other characteristics
such as slow return to baseline, overshoots, or
“shoulders

40. Category II FHR tracing
• Category II FHR tracings are INDETERMINATE
• NOT predictive of abnormal fetal acid-base
status
• Requires continued surveillance and
interpretation in light of entire clinical
information

41. CATEGORY II MANAGEMENT
• Both responses are highly predictive of normal
fetal acid–base status and, thus, may help guide
clinical management
1) Moderate FHR Variability
2) The presence of FHR accelerations
-spontaneous
-digital scalp stimulation
-vibroacoustic stimulation

42. CATEGORY II MANAGEMENT
Recurrent Variable decelerations
Prolonged Decelerations
Bradycardia
GOAL
Alleviate umbilical cord compression
Amnioinfusion
?PROLAPSED CORD?
DOES NOT HELP WITH LATE DECELERATIONS

43. Category III FHR tracing
ABSENT FHR VARIABILITY
AND
• Recurrent late decelerations
• Recurrent variable decelerations
• Bradycardia
OR
SINUSOIDAL PATTERN

44. Category III FHR tracing
• Category III FHR tracings are abnormal
• Predictive of abnormal fetal acid-base status at time
of observation
• Require prompt evaluation
• Depending on situation, efforts may include:
– Maternal oxygen( 10 liter per mask)
– Maternal position change
– Discontinuation of labor stimulation
– Treatment of maternal hypotension
– AFTER CORRECTIVE ATTEMPT make an effort to TO
DEMONSTARTE FETAL HEART RATE ACCELERATION BY
FETAL DIGITAL SCALP STIMULATION OR FAS
STIMULATION TO DOWN GRADE BACK TO CATEGORY II

45. Promote Oxygenation
and
Improve blood flow
• Minimal or Absent FHR variability
• Recurrent late decelerations
• Prolonged decelerations
• Bradycardia
INITIATE
• Lateral positioning (either left or right)
• Oxygen administration
• IV fluid bolus
• Reduce uterine contraction frequency

48. NICHD Expert Panel
Agreement about definition of NORMAL FHR tracing that confers an
extremely high predictability of a NORMALLY oxygenated fetus when it is
obtained
• Normal baseline rate
• Moderate FHR variability
• Presence of accelerations
• Absence of decelerations
Agreement that patterns predictive of current or impending fetal asphyxia
PLACING the fetus is at risk for NEUROLOGIC DAMAGE OR DEATH
ABSENT FHR VARIABILITY
AND
RECURRENT LATES
RECURRENT VARIABLES

49. Goals of EFM
• Delivery of newborn
– In the absence of a significant acidosis
• Umbilical artery pH < 7.1, base excess < -12
• And/or 5 minute Apgar < 7
– In the presence of neonatal vigor
• Quickly categorize FHR patterns based on their
relationship (or lack thereof) to the above goals
• Clearly communicate FHR patterns to members
of the OB team

50. Communication
• SBAR
– Situation (patient characteristics)
– Background (evolution of tracing)
– Assessment (description of current tracing)
– Recommendation (action plan)

51. Communication
• Description of FHR pattern
– VARIABILLITY (absent, minimal, moderate, marked)
– Descriptions of PERIODIC/EPISODIC changes
• Type or shape
• Recurrent or intermittent
• Severity (nadir)
• Relationship to uterine activity
– BASELINE FHR
– Presence/absence of ACCELERATIONS
– Has the FHR tracing changed or evolved over time
since admission. Is the change transient with an
obvious cause ( meds, hypotension, meconium,
AROM, fever, bleeding, maternal position)
– Potential influence of Maternal condition &/OR Fetal
condition in relation to FHR patterns

52. DESCRIPTION FOR SBAR
– RATE
(Tachycardia or increase in baseline >/ = to 15 bpm from
admission)
– VARIABILITY
(loss of variability with change in fetal maternal condition)
– ACCELERATIONS (spontaneous or stimulated & 15 bpm or
less )
– PERIODIC/EPISODIC DECELERATIONS
– Changes of FHR OR PATTERN OR MATERNAL CONDITION
COMPARED TO ADMISSION OR SIGNIFICANT TIME FRAME

58. SBAR THIS STRIP

59. SBAR THIS STRIP

60. SBAR THIS STRIP

61. ETILOGY OF CP

62. Prematurity results in CP
• CP develops in as many as 15-20 % of surviving premature infants
• The earlier the gestational age at delivery; The greater is the risk
of developing CP.
• CP risk % >>> 30 weeks >> 32-34 weeks with a plateau > 34
weeks unless chorioamnionitis or intrapartum hypoxia occurs.
• CP as a result of prematurity is associated with the presence of
Periventricular Leukomalacia (PVL is an anatomic lesion.)
• In addition to perinatal inflammation, cerebral ischemia contributes
to PVL and may result in CP in preterm infants.
• Other conditions that primarily affect preterm infants and may lead
to CP include severe intraventricular hemorrhage (IVH) and
periventricular hemorrhagic infarction which may result in
posthemorrhagic hydrocephalus which frequently leads to CP

63. Chorioamnionitis SYNERGISTICALLY
Increases the risk of CP with Prematurity
• There are significant associations between clinical chorioamnionitis or
histological chorioamnionitis and cerebral palsy, for clinical
chorioamnionitis a pooled odds ratio of 2.42 (95% CI 1.52–3.84), and for
histological chorioamnionitis a pooled odds ratio of 1.83 (95%
confidence interval, 1.17–2.89).
• This data is associated with an increased risks of 140% and 80% for
neonates exposed to clinical chorioamnionitis or histological
chorioamnionitis, to develop CP respectively.
• PVL occurs more frequently in premature infants born to mothers with
chorioamnionitis, premature or prolonged rupture of the membranes. In
a meta-analysis, chorioamnionitis was associated with cystic PVL
(relative risk 3.0) and cerebral palsy (relative risk 1.9) . Funisitis or
neonatal sepsis also increases the risk of PVL
Obstet Gynecol 2010;116:387–92 Clin Obstet Gynecol 1998 Dec;41(4):827-31
.
Paediatr Perinat Epidemiol 1998 Jan;12(1):72-83

64. < 5 % of CP results from
Intrapartum Hypoxia
Obstet Gynecol. 2006 Jun;107(6):1357-65.
• Data were available for analysis in 213 cases of CP. Major antenatal or
pediatric cerebral palsy-related pathologies were identified in 98.1% of all
these cases. An isolated acute intrapartum hypoxic event was defined as
likely in only 2 of the 46 neonates born at term and none born preterm.
• CONCLUSION: Cerebral palsy was seldom preceded by acute intrapartum
hypoxia but antenatal cerebral palsy-related pathologies are often
detectable. The objective American College of Obstetricians and
Gynecologists/American Academy of Pediatrics criteria are useful to audit
cerebral palsy causation and exclude primary intrapartum hypoxia