[OBSTETRICS A] INTRAPARTUM ASSESSMENT

INTRAPARTUM ASSESSMENT
Dr. San Jose

 Nowadays, almost all women undergo electronic fetal

heart rate monitoring during labor. It used to be that this
was introduced only to those who were high risk.

INTERNAL ELECTRONIC FETAL HEART RATE MONITORING

 Fetal Heart Rate is measured by attaching a bipolar spiral
electrode that penetrates the fetal scalp

 This means that the bag of water is to be ruptured

 A small incision is made to attach the spiral
electrode to the scalp (Picture Above) FETAL ECG (SCALP ELECTRODE):
PREMATURE ATRIAL CONTRACTION
 P wave, QRS complex and T wave is amplified  Sometimes, if the time interval from one R to the next R
 R wave voltage is shorter, it may be due to heart rate acceleration 
 Portion of the ECG most reliably detected May be interpreted as Premature Atrial Contraction
(PAC)
 t2  Shorter = Premature Atrial Contraction

EXTERNAL (INDIRECT) ELECTRONIC FETAL HEART RATE

MONITORING
 Fetal Heart Rate is detected through the maternal
abdominal wall using UTZ Doppler principle

 This is a non-invasive technique of electronic fetal

heart rate monitoring
 Most commonly used in most hospitals
(Picture Above) INTERNAL ELECTRONIC FETAL HEART RATE - You do not have to rupture the bag of water
MONITORING - You do not have to puncture the scalp and attach
 Electrode is attached to the fetal scalp  Attached to the the fetal electrode
cardiac monitor
 Consist of a transducer that emits UTZ and a sensor to detect
 Cardiac monitor will register the FHR pattern
a shift in frequency of the reflected sound
 F: Fetal heart wave secondary to fetal heart rate
 Coupling gel must be applied because air conducts UTZ
 M: Maternal heart rate  Weaker one
poorly
 Although the scalp electrode is attached to the fetus,
because of the loud sound produced by the maternal
heart rate, this can also be reflected. But since
electrode is attached to the fetal scalp, then,
understandably, this fetal heart pattern should be
more prominent
 However, if the fetus is dead and the scalp lead is
attached to the fetus, then the maternal heart sounds
will be louder and more prominent, and you will not
be able to appreciate the fetal heart rate at all.

 Time (t) in Milliseconds  Time interval between two R-

waves
 Premature Atrial Contraction  Heart rate acceleration
when the interval (t2) is shorter than the preceding one
 Beat to Beat Variability  Phenomenon of continuous R-to- (Picture Above) EXTERNAL (INDIRECT) ELECTRONIC FETAL
R wave fetal heart rate computation HEART RATE MONITORING

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 Doppler is placed on the abdomen to where the fetal  30 beats per minute/per vertical cm (30-240 beats/min)
heart tones are most audible.  3 cm/min chart recorder paper speed

 We use the faster 3cm/min paper speed rather than

the slower 1cm/min paper speed because the slower
 AUTOCORRELATION
1cm/min paper speed will not reflect the variations in
 Reflected UTZ signals from moving fetal heart valves are
the fetal heart rate pattern.
analyzed through a microprocessor that compares
incoming signals with the most recent previous signal
 Based on the premise that the FHR has regularity whereas BASELINE FETAL HEART ACTIVITY
“noise” is random without regularity  Refers to the modal characteristics that prevail apart from
periodic accelerations or decelerations associated with
 Before the cardiac tracing appears on the togograph
uterine contractions
paper, electronic editing is done by the monitor
 Beat-to-Beat variability, Fetal Arrhythmia
 Noise will be eliminated and what will be seen in
the cardiotocogram will be the fetal tracing  Beat-to-Beat Variability  Also same as baseline fetal
heart activity
DISADVANTAGES  Sinusoidal or Saltatory Fetal Heart Rates
INTERNAL ELECTRONIC EXTERNAL ELECTRONIC  Normal Baseline FHR  110-160 beats/min
FETAL HEART RATE FETAL HEART RATE
MONITORING MONITORING BRADYCARDIA
 Necessitates membrane  Does not provide the  FHR <110 beats per minute
rupture and uterine precision of FHR  Mild = 100 – 119 (No fetal compromise)
invasion measurement or the  Moderate = 80 – 100
quantification of uterine
 Severe = <80 lasting for 3min
pressure afforded by
internal monitoring
POSSIBLE CAUSES OF FETAL BRADYCARDIA:
 Congenital Heart block
 Internal Electronic FHR Monitoring
 Fetal Compromise
 More accurate
 Maternal Hypothermia
 External Electronic FHR Monitoring
 Severe Pyelonephritis
 Non-invasive procedure  Less prone to
complications
 Maternal Hypothermia
 Usually during general anesthesia
SCALING FACTORS
TACHYCARDIA
 FHR > 160 beats per minute
 Mild = 161-180
 Severe = >180

POSSIBLE CAUSES OF FETAL TACHYCARDIA:

 Maternal Fever
 Maternal Infection
 Fetal Compromise
 Cardiac Arrhythmias
 Administration of Parasympathetic Drugs (Atropine)
 Sympathomimetic Drugs (Terbutaline)

(Picture Above) Fetal heart rate obtained by scalp  Maternal Fever

electrode (upper panel) and recorded at 1 cm/min  Most commonly due to premature rupture of
compared with that at 3 cm/min chart recorder paper membrane leading to chorioamnionitis
speed. Concurrent uterine contractions are shown (lower
panel).  Key features to distinguish fetal compromise in association
w/ tachycardia  Concomitant Heart Rate Decelerations

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 Fetal tachycardia or bradycardia alone may not 4. Marked Variability

indicate fetal compromise specially if it is mild to
moderate, but if this is accompanied by concomitant ABSENT VARIABILITY
heart rate decelerations, then this is indicative
already of fetal compromise.

BEAT TO BEAT VARIABILITY

 BASELINE VARIABILITY  You will notice that it is almost a flat tracing  No
 An important index of cardiovascular function, regulated oscillations
by autonomic nervous system (sympathetic and  If this is accompanied by fetal bradycardia  Baby is
parasympathetic push-pull) compromised
 Produces beat-to-beat or moment-to-moment oscillation
of the baseline FHR
MINIMAL VARIABILITY
 SHORT TERM VARIABILITY

 ≤ 5 beats per minute

MODERATE VARIABILITY
 Instantaneous change in FHR from 1 beat to the next
 Measure of time interval between cardiac systoles
 Measured only with scalp electrodes

 LONG TERM VARIABILITY  NORMAL

 6-25 beats per minute

MARKED VARIABILITY

 Oscillatory changes in 1 minute

 Normal Frequency of Waves = 3-5 cycles per minute
 Normal Beat-to-beat Variability = 6-25 beats per minute  > 25 beats per minute

 Long term variability shows waviness of the pattern  This may mean that the fetus is compromised
 Short term variability shows abrupt change of the fetal
heart rate
 INCREASED VARIABILITY
 Fetal Breathing
 DETERMINANTS OF BASELINE FETAL HEART RATE ACTIVITY  Fetal Body Movements
 Autonomic Nervous System  Advancing Gestations
- Sympathetic  Accelerator influence - ≤ 30 weeks
- Parasympathetic  Decelerator factor (vagal)  Same variability during rest and activity
 Arterial Chemoreceptors - > 30 weeks
- Hypoxia and hypercapnia can modulate rate  Increased variability during activity
 Decreased variability at rest
 TYPES OF VARIABILITY - Fetal Gender  No effect on FHR variability
1. Absent Variability
2. Minimal Variability  DECREASED VARIABILITY
3. Moderate Variability  <5 beats per minute excursion from baseline

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 Causes: PERIODIC FETAL HEART RATE CHANGES

- Analgesics  Deviation from baseline related to uterine contractions
- CNS Depressant Drugs  Acceleration  Increase above baseline
- Magnesium Sulfate  Deceleration  Decrease below baseline
 If you stop using these 3, variability will be EARLY DECELERATION
reversed
 Significance:
- Maternal Acidemia  HEAD COMPRESSION

 Vagal nerve stimulation due to

dural stimulation that
mediates the heart rate

 “Mirror image effect”

 Deceleration starts at the beginning contraction
 Persists for at least 30 seconds
 Other Causes of Decreased Variability:  Drops to a nadir at the acme of the contraction
- Analgesics during labor  Recovers at the end of the contraction
- CNS Depressant Drugs
 Narcotics
 Barbiturates LATE DECELERATION
 Phenothiazines  Significance:
 Tranquilizers  UTEROPLACENTAL
 General Anesthetics INSUFFICIENCY
 Magnesium Sulfate  Maternal
Hypotension
 Diminished Variability x 1 hour  Diagnostic of  Excessive Uterine
Developing Acidemia and Imminent Fetal Death Activity
 Loss of Variability + Deceleration = FETAL ACIDEMIA  Placental Dysfunction
 Reduced Baseline Heart Rate Variability  OMINOUS
SIGN  Deceleration starts at the peak or acme of the
- SINGLE MOST RELIABLE SIGN OF FETAL COMPROMISE contraction
 Persists for at least 30 seconds
 SINUSOIDAL PATTERN  Drops to a nadir at the end contraction
 Recovers in between contractions

 Smooth pattern of regular fluctuation

 Fetal Anemia:
- D-Isoimmunization
- Ruptured Vasa Previa
- Fetomaternal Hemorrhage
- Twin-twin Transfusion
- Fetal Intracranial Hemorrhage
- Fetal Asphyxia
 Baseline FHR 120-160 beats/minute + Regular Oscillations
 Amplitude: 5-15 beats/minute
 Long term variability frequency = 2-5 cycles per minute
 Fixed short term variability
 Sinusoidal waveform
 Absence of accelerations

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 If you are doing Oxytocin Challenge Test and you see  Rapidly recurring couplets of accelerations combined with
Late Decelerations  STOP Oxytocin administration deceleration
 This can lead to excessive uterine activity  Significance: Cord Compression
 Do not signal fetal compromise if not associated with other
FHR findings
VARIABLE DECELERATION
 Significance: PROLONGED DECELERATION
 CORD COMPRESSION
 Abrupt changes in rate
 Jagged appearance
 Onset varies with successive
contractions
 Pathologic: < 70 beats per
minute lasting for more than 60 seconds

 Deceleration could happen at the beginning of the

contraction, at the peak of the contraction, or in between
contractions

 PARTIAL AND COMPLETE OCCLUSION OF THE UMBILICAL

CORD

 Isolated deceleration lasting 2 minutes or longer but less

than 10 minutes from onset to return to baseline
 Causes:
 Cervical Exam
 Uterine Hyperactivity
 Maternal Supine Hypotension
 Cord Enlargement
 Epidural, Spinal, or Paracervical Anesthesia
 Maternal Hypoperfusion or Hypoxia
 Usually self-limited if the insult does not recur immediately
 May be followed by:
 Loss of beat-to-beat variability
 Partial Occlusion  Acceleration  Baseline tachycardia
 Complete Occlusion  Deceleration  A period of late decelerations
Resolve as the fetus recovers
SALTATORY PATTERN
FETAL HEART RATE PATTERNS DURING 2ND STAGE LABOR
 Causes of Deceleration and Baseline Bradycardia:
 Cord Compression
 Fetal Head Compression

 During the 2nd stage of labor, this is when the head

of the fetus try to navigate the bony pelvis  Head
Compression

 Characteristic of 2nd Stage Variable Deceleration:

 As the total number of decelerations of <70 beats per
minute increased, the 5-minute APGAR score decreased

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 Patterns Associated With Increased Fetal Compromised pH MANAGEMENT

(MEMORIZE!) > 7.25  Observe labor
 Loss of beat-to-beat variability + Baseline Fetal Heart Rate 7.20 – 7.25  Repeat measurement after 30 minutes
< 90 beats per minute  Repeat measurement immediately
 Persistent or progressive baseline bradycardia or <7.20
 Prompt delivery if the low pH is confirmed
tachycardia were associated with low APGAR scores
 Abrupt Fetal Heart Rate deceleration to <100 beats per
minute + Loss of beat-to-beat variability for 4 minutes or
longer
 Abnormal baseline Fetal Heart Rate +/- Absent beat-to-
beat variability + 2nd Stage Decelerations

ADMISSION FETAL MONITORING IN LOW-RISK PATIENTS

 Low risk pregnancies are monitored for a short period on
admission

 All women in labor undergo baseline

cardiotopography
 If the pattern is abnormal  Proceed with FETAL SCALP BLOOD SAMPLING
continuous electronic FHR monitoring
 If normal  May just use ordinary stethoscope SCALP STIMULATION
 Alternative to Scalp Blood Sampling
 Continuous monitoring is used only if abnormalities of the  Acceleration of heart rate in response to pinching the scalp
FHR are subsequently identified with an allis clamp was invariably associated with normal pH
 Resulted in increased interventions (Operative Delivery)  Failure to provoke acceleration was not uniformly predictive
of fetal academia
COMPLICATIONS OF ELECTRONIC FETAL MONITORING
 Application at other sites than the scalp or breech may prove VIBROACOUSTIC STIMULATION
serious  Substitute for Fetal Scalp Sampling
 Fetal vessel in the placenta may be ruptured by catheter  Involves use of an electronic artificial larynx placed onto the
placement maternal abdomen
 Cord compression from entanglement with the catheter  Effective predictor of fetal acidosis in the setting of variable
 Penetration of the placenta, causing hemorrhage and decelerations
possibly uterine perforation during catheter insertion  Predictability for fetal acidosis is limited in the setting of late
 Increased risk of infection decelerations
 NORMAL
RELATIVE CONTRAINDICATIONS TO INTERNAL FETAL HEART  If FHR acceleration at least 15 beats per minute for at least
RATE MONITORING 15 seconds occurs within 15 seconds after the stimulation
 HIV and with prolonged fetal movements
 Herpes Simplex Virus
 Hepatitis B Virus FETAL PULSE OXIMETRY
 Hepatitis C Virus  Reliably register fetal
oxygen saturation in 70-
 This may cause vertical transmission of the infection to 95% of women
the fetus. throughout 50-88% of
 If you rupture the bag, you allow these viruses to enter their labors
the fetus  Lower limit for Normal
Fetal Oxygen Saturation
= 30%
OTHER INTRAPARTUM ASSESSMENT TECHNIQUES
FETAL SCALP BLOOD SAMPLING  Brief, transient fetal
oxygen saturation below 30% when persistent for 2 minutes
 Measurement of the pH in capillary scalp blood to identify
or longer were associated with increased risk of potential
the fetus in serious distress
fetal compromise
 BENEFITS: Fewer Cesarean deliveries for fetal distress
 No neonatal benefits or adverse effects associated with
fetal pulse oximetry

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FETAL ECG TRUE FETAL DISTRESS PATTERNS

 As fetal hypoxia worsens, there are changes in the ST  0 Beat-to-beat variability + Severe Decelerations or Baseline
segment and PR interval of the fetal ECG FHR <110 beats/minute x 5 minutes or longer
 ST abnormalities may occur late in the course of fetal
compromise MANAGEMENT FOR NONREASSURING FHR PATTERN
 Maybe useful in preventing fetal acidosis & encephalopathy  Reposition patient
with abnormal standard FHR
 Left lateral position
INTRAPARTUM DOPPLER VELOCIMETRY
 Discontinue uterine stimulants and correction of uterine
 Abnormal waveforms may signify pathological umbilical-
hyperstimulation
placental vessel resistance
 Vaginal exam
 Poor indicator of adverse perinatal outcome
 Correction of maternal hypotension
 Not useful for either antepartum or intrapartum  Notify anesthesiologist and nursing staff of need for
assessment emergency delivery
 Only useful in the setting of fetal growth restriction  Continuous FHR monitoring
 Qualified pediatric care
 Had little role in fetal surveillance during labor  Give oxygen

FETAL DISTRESS MANAGEMENT OPTIONS WITH “FETAL DISTRESS” (Not discussed)

 REASSURING  AMNIOINFUSION
 Suggests restoration of confidence by a particular pattern  3 Clinical Areas:
 NONREASSURING - Treatment of variable or prolonged decelerations
 Suggests inability to remove doubt - Prophylaxis for women with oligohydramnios as with
prolonged ruptured membranes
DIAGNOSIS OF FETAL DISTRESS - Dilute or wash out thick meconium
 Based on fetal heart rate patterns can be imprecise and  Protocol
controversial - 500-800 mL bolus warmed NSS followed by continuous
 Ayres-de-Campos & Colleagues infusion of 3 mL per minute
 Investigated interobserver agreement of fetal heart rate  Complications
interpretation – Normal, Suspicious, or Pathological - Uterine hypertonus
 Agreed on 62% normal, 42% suspicious, 25% pathological - Abnormal FHR tracing
 Fetal Distress Group - Amnionitis
 With zero variability plus late or moderate to severe - Cord Prolapse
variable deceleration or with baseline rates <110 - Uterine Rupture
beats/minute for 5 minutes or more - Maternal Cardiac or Respiratory Compromise
 Parer & Ikeda (2007)  Developed a framework for - Placental Abruption
standardized mechanism of intrapartum fetal heart rate - Maternal Death
patterns (134 pattern and color-coded each pattern):
 GREEN  For those without threat of academia and no NATIONAL INSTITUTES OF HEALTH WORKSHOPS
intervention was required THREE-TIER CLASSIFICATION SYSTEM
 RED  With severe threat of academia and rapid delivery  Categorizations of fetal heart rate interpretation into a
was recommended THREE-TIER System:
 Category I: NORMAL
DIAGNOSIS OF FETAL DISTRESS Includes all of the following:
PATTERN INTERPRETATIONS - Baseline Rate: 110-160 beats per minute
 Baseline: 110-160 beats per minute - Baseline FHR variability: Moderate
 Variability: 6-25 beats per minute - Late or Variable Decelerations: Absent
NORMAL - Early Decelerations: Present or Absent
 Accelerations present
 No decelerations - Accelerations: Present or Absent
INTERMEDIATE  No consensus
 Category II: INDETERMINATE
 Recurrent late or variable
- All fetal heart tracings not categorized as 1 or 3
SEVERELY decelerations with zero variability
- May represent big fraction of clinical cases
ABNORMAL  Substantial bradycardia with zero
- Baseline Rate:
variability
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 Bradycardia not accompanied by absent baseline  Early imaging study showing evidence of acute nonfocal
variability cerebral abnormality
 Tachycardia
- Baseline FHR Variability: 3 CATEGORIES OF BRAIN DAMAGE FOLLOWING AN
 Minimal baseline variability ASYPHYXIAL EVENT (Not discussed)
 Absent baseline variability not accompanied by
recurrent decelerations •Neuronal necrosis with pyknosis or lysis of the
 Marked baseline variability 18-48 nucleus in shriveled eosinophilic cells
hours
- Accelerations:
 Absence of induced acceleration after fetal
stimulation •More intense neuronal macrophage response
48-72
- Periodic or Episodic Decelerations: hours
 Recurrent variable deceleration accompanied by
minimal or moderate baseline variability •All the preceding + astrocytic response with
 Prolonged deceleration  2 minutes but < 10 minutes More than gliosis and early cavitation
3 days
 Recurrent late decelerations with moderate baseline
variability
 Variable deceleration with other characteristics such
as slow return to normal, “overshoots”, “shoulders”
GUIDELINES FOR INTRAPARTUM FETAL HEART RATE
SURVEILLANCE
 Category III: ABNORMAL LOW RISK HIGH RISK
Include either: SURVEILLANCE
PREGNANCIES PREGNANCIES
- Absent baseline FHR variability and any of the following: Intermittent
 Recurrent late decelerations Yes Yes
Auscultations
ACCEPTABLE
 Recurrent variable decelerations Continuous
METHODS
 Bradycardia Electronic Yes Yes
- Sinusoidal pattern Monitoring
1st Stage
CRITERIA TO DEFINE AN ACUTE INTRAPARTUM HYPOXIC Labor 30 minutes 15 minutes
EVALUATION
EVENT AS ASUFFICIENT TO CAUSE CEREBRAL PALSY (Active)
INTERVALS
(Not discussed) 2nd Stage
15 minutes 5 minutes
ESSENTIAL CRITERIA (Must meet all 4) Labor
 Evidence of metabolic acidosis in fetal umbilical cord arterial
blood obtained at delivery (pH <7 and base deficit  12 INTRAPARTUM SURVEILLANCE OF UTERINE ACTIVITY
mmol/L)  INTERNAL UTERINE PRESSURE MONITORING
 Early onset of severe or moderate neonatal encephalopathy  Amniotic fluid pressure is measured between and during
in infants born at  34 weeks AOG contractions by a fluid-filled plastic catheter with its distal
top located at the presenting part
 Cerebral palsy of spastic quadriplegic or dyskinetic type
 Exclusion of other identifiable etiologies
 EXTERNAL MONITORING
 Trauma
 Uses displacement transducer held against the abdominal
 Coagulation Disorders
wall
 Infectious Conditions
 Can give good indication of the onset, peak, and end of
 Genetic Disorders
contraction
CRITERIA THAT COLLECTIVELY SUGGEST INTRAPARTUM
TIMING (Within 0-48 hours of delivery but are nonspecific to  PATTERNS OF UTERINE ACTIVITY
asphyxia insults)  Uterine performance is the product
 Sentinel hypoxic event occurring immediately before or of the intensity – Increased uterine
during labor MONTEVIDEO pressure above baseline – of a
UNITS contraction in mmHg multiplied by
 Sudden and sustained fetal bradycardia or absence of FHR
variability in presence of persistent, late, or variable contraction frequency per 10
decelerations, usually after a hypoxic sentinel event when minutes
pattern was preciously normal  Typical increase in uterine activity in
PRELABOR
 APGAR scores 0-3 beyond 5 minutes the last weeks of pregnancy
 Onset of multisystem involvement within 72 hours of birth

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CLINICAL  Commence at 80-120 montevideo

LABOR units
 Increase from 25mmHg to 50mmHg
1ST STAGE  Frequency increase from 3-5
LABOR contractions per 10 minutes
 Uterine base tone 8-12 mmHg
 80-100 mmHg
2ND STAGE
 Frequency of 5-6 per 10 minutes
LABOR
 Duration 60-80 seconds

 Intensity of Uterine Contraction that is Clinically Palpable

 10mmHg
 Intensity of Uterine Contraction Associated with Pain
 >15 mmHg
 This is the minimum pressure require for distending the
lower uterine segment and cervix
 Uterine Contractions After Birth
 Identical to those resulting in the delivery of the infant

ORIGIN AND PROPAGATION OF CONTRACTIONS

 Normal contractile wave originates near the uterine end of
one of the fallopian tubes, usually the right, propagates
towards the cervix
 Contraction Spread = 2 cm/second
 Whole organ depolarized in 15 seconds
 Intensity greatest in the fundus and diminishes in the lower
uterus
 Descending gradient of pressure serves to direct fetal
descent and efface the cervix

INCOORDINATION (Not discussed)

 A contractile wave being in one comual-region but does not
synchronously depolarize the entire uterus. As a result,
other contraction begin in the contralateral pacemaker and
produces the 2nd contractile wave of the couplet.
 Typical of early labor

HYPOTONIC CONTRACTIONS (Not discussed)

 Contraction intensity <25 mmHg
 Frequency <2 per 10 minutes
 Slow progress of labor

NORMAL LABOR (Not discussed)

 Minimum of 3 contractions >25 mmHg and <4 minute
interval between contractions
 Lesser amount associated with arrest of active labor

UTERINE CONTRACTION PRESSURES IN WOMEN AT TERM

GIVEN OXYTOCIN (Not discussed)
 200-225 and up to 300 Montevideo units to effect delivery
(should be sought before doing CS for presumed dystocia) Thank you Zyrine Carpeso and Nicollete Castillo for the pictures +
Thank you Raymond Gonzales for encoding 

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