Intrapartum Fetal Surveillance

Yesuneh(MD)
 Outline of Presentation
• Objective • History of fetal monitoring
• Introduction development
• Physiologic control of FHB • Comparison of EFM and
• Transfer of oxygen from internal fetal monitoring
environment to fetus • Fetal heart rate changes-
• Fetal Response To baseline and periodic
Interrupted Oxygen Transfer • Three tiered fetal heart rate
• Fetal acid base balance interpretation
• History of fetal monitoring • Management of NRFS
development • Reference
 Objective
• The objective of intrapartum FHR monitoring
is to prevent:-

 Fetal injury that might result from interruption

of normal fetal oxygenation during labor.
PHYSIOLOGIC BASE OF HYPOXIA
 Introduction

• Normal human labor is characterized by

rhythmic uterine contractions that
intermittently interrupt the transplacental
passage of oxygen from the mother to the
fetus.
• These brief episodes of transient interruption
of oxygenation are tolerated without
consequence by almost all fetuses.
 Introduction cont…
• In a very small subset, however, severe fetal
oxygen deficiency can lead to hypoxic injury or
even death.
• The heart rate is the result of many
physiologic factors that modulate the intrinsic
rate of the fetal heart, the most common of
which are signals from the ANS.
PARASYMPATHETIC NERVOUS SYSTEM

• PNS consists primarily of the vagus nerve,

which originates in the medulla oblongata.
• The vagus nerve innervates the SA and AV
nodes.
• The vagus nerve therefore has two possible
effects on the heart:
 A tonic influence tending to decrease FHR and
 An oscillatory influence that results in FHR
variability.
 SYMPATHETIC NERVOUS SYSTEM
• SNS are widely distributed in the muscle of the
heart at term.
• Stimulation of the SNS releases NE and
increases the rate and strength of fetal cardiac
contractions, resulting in higher cardiac
output.
• Blocking the action of these SNS causes a
decrease in FHR of approximately 10
beats/min.
 Effect of gestational age on FHR
• Advancing gestational age is associated with
slowing of the baseline heart rate.

• Advancing gestational age is also associated

with increased frequency and amplitude of
FHR accelerations, which are modulated by
the SNS.
 CHEMORECEPTORS
• Chemoreceptors are found in the
 Peripheral (aortic and carotid bodies)
 CNS (medulla oblongata)
• The net result of hypoxia or hypercapnia in
the fetus is bradycardia with hypotension.
 BARORECEPTORS
• Found in the arch of the aorta and in the
carotid sinus
• Sensitive to increases in blood pressure.
• This is an extremely rapid response, occurring
almost with the first systolic rise of blood
pressure.
 CENTRAL NERVOUS SYSTEM

• When the fetus is sleeping, body movement

slows, and FHR variability decreases,
suggesting an association between these two
factors and CNS activity.
 HORMONAL REGULATION
• Adrenal Medulla
 The fetal adrenal medulla produces E and NE in response to stress.
 Both substances act on the heart and CVS to produce a faster FHR.
• Renin-Angiotensin System
 AG II may play a role in fetal circulatory regulation at rest.
 Its main activity is observed during hemorrhagic stress on a fetus.
• Prostaglandins
 Their main roles with respect to CVS function are in:-
 Regulating umbilical blood flow and
 Maintaining the patency of the DA during fetal life.
TRANSFER OF OXYGEN FROM THE
ENVIRONMENT TO THE FETUS
 External Environment
• Oxygen comprises approximately 21% of
inspired air.
• As oxygen is transferred from the external
atmosphere, the partial pressure progressively
declines.
• By the time oxygen reaches fetal umbilical
venous blood, the partial pressure may be as
low as 30 mm Hg.
 Maternal Lungs
• At sea level, alveolar PO2 is approximately 100
to 105 mm Hg.
• From the alveoli, oxygen diffuses across a thin
blood-gas barrier into the pulmonary capillary
blood.
 Lungs
• Interruption of oxygen transfer from the
environment to the alveoli can result from:-
 Airway obstruction or
 Respiratory Depressant (Narcotics,
Magnesium)
 Convulsions (Apnea).
 Lungs
• Interruption of oxygen transfer from the alveoli
to the pulmonary capillary blood can be caused
by:-V/Q mismatch and diffusion defects due to
conditions such as
 Pulmonary embolus,
 Pneumonia,
 Asthma,
 Atelectasis, or
 Acute respiratory distress syndrome (ARDS).
 Interruption of oxygen transfer from the environment to the fetus at the
level of the maternal heart can be caused by:-

• Arrhythmia, Hypertension
• Hypovolemia, Valvular stenosis,
• Compression of the IVC, Valvular insufficiency,
• IHD, PHTN,
• Diabetes, Coarctation of the aorta
• Cardiomyopathy,
• CHF
 Maternal Vasculature
 Hypotension caused by  Chronic hypertension,
regional anesthesia,  Longstanding diabetes,
 Hypovolemia,  Collagen vascular
 Impaired venous return, disease,
 Impaired cardiac  Thyroid disease, or
output, or  Renal disease
 Medication. • Preeclampsia
 Uterus
• Interruption of oxygen transfer from the
environment to the fetus at the level of the
uterus commonly results from

 Tetanic Uterine contractions

 Elevated baseline uterine tone
 Uterine rupture
 Placenta
• Many conditions can interfere with the
transfer of oxygen across the placenta.

 Placental abruption or
 Bleeding placenta previa or
 Vasa previa,
 Fetal Blood
• After oxygen has diffused from the intervillous space
fetal anemia and
• Reduced oxygen carrying capacity secondary to
 Alloimmunization,
 Hemoglobinopathy,
 G6PD,
 Viral infections,
 Fetomaternal hemorrhage,
 Methemoglobinemia,
 Bleeding vasa previa.
 Umbilical Cord
• At the level of the umbilical cord:-
 Mechanical compression.
 Vasospasm,
 Thrombosis,
 Atherosis,
 Hypertrophy,
 Hemorrhage,
 Inflammation, or
 True “knot.”
 FETAL RESPONSE TO INTERRUPTED
OXYGEN TRANSFER

• Interruption of oxygen transfer at any point

along the oxygen pathway may result in
progressive deterioration of fetal oxygenation.

• The cascade begins with hypoxemia,

(Umbilical Artery PaO2 < 15 to 25 mm Hg)
INTERRUPTED OXYGEN TRANSFER
• Recurrent or sustained hypoxemia can lead to
decreased delivery of oxygen to the tissues
(hypoxia).
• Tissues may be forced to switch from aerobic
to anaerobic metabolism, results in the
production of lactic acid.
• Accumulation of lactic acid in the tissues
results in metabolic acidosis.
INTERRUPTED OXYGEN TRANSFER
• If the buffering capacity is exceeded, leading
to metabolic acidemia.
• Recurrent or sustained hypoxia and acidosis in
the peripheral tissues can lead to
 Loss of peripheral vascular tone,
 Reduced peripheral vascular resistance,
 Hypotension, and
 Hypoxic-ischemic injury to critical tissues and
organs,
 Effects of Labor
• Each uterine contraction transiently
diminishes
 Uterine blood flow,
 Reduces placental perfusion, and
 Impairs transplacental gaseous exchange.
UMBILICAL CORD BLOOD ACID-BASE ANALYSIS

• Acid-base analysis of umbilical cord blood

provides an objective method of evaluating a
depressed newborn’s condition, especially
with regard to hypoxia and acidemia.
• There is no consensus about the most
appropriate umbilical artery pH cutoff for
defining acidemia,
 Pathologic Fetal Acidemia
• What level of UA pH should be considered
abnormal, pathologic, or clinically significant?
• The former pH cutoff of 7.20 is no longer
considered appropriate.
• Evidence suggests that significant morbidity is
more likely among neonates with umbilical
artery pH values lower than 7.00, especially if
associated with a low Apgar score (≤3).
 MEASURING ACID-BASE STATUS
• The ACOG recommends umbilical cord blood acid-
base analysis in the following situations:
 Cesarean delivery for fetal compromise
 Low 5-minute Apgar score
 Severe growth restriction
 Abnormal FHR tracing
 Maternal thyroid disease
 Intrapartum fever
 Multifetal gestations
FETAL MONITORING
 BRIEF HISTORY OF FETAL MONITORING

• Auscultation of the fetal heart was described

in the medical literature as early as the 18TH
century.
• In 1917, Hillis described the modified
stethoscope known today as the De Lee-Hillis
fetoscope.
• In 1906, Cremer recorded the first fetal
electrocardiogram (ECG).
 BRIEF HISTORY Cont..
• The concept of direct application of the ECG
electrode to the fetus in utero was introduced
in the 1950s.
• Edward Hon “father of EFM” instantaneous
recording of the fetal ECG from the maternal
abdomen.
• EFM use in labor is most common currently
from mid 1970s
 INSTRUMENTATION
• The fetal monitor tracing is a continuous
paper strip comprising two Cartesian graphs.
• The upper graph displays an instantaneous
recording of the FHR.
• Uterine activity is displayed on the lower
graph.
 Direct FHR and Uterine Activity Monitoring

• Direct FHR monitoring involves

 Transcervical application of an ECG electrode
to the fetus,
 Dilation of the cervix,
 Rupture of the membranes, and
 Access to the fetal presenting part.
Indirect FHR and Uterine Activity Monitoring

• Indirect (external) monitoring does not

require the trans-cervical placement of
electrodes or catheters.
• Consequently, external FHR monitoring uses
an ultrasound transducer applied with straps
to the maternal abdomen and can be
performed prior to labor.
 Characteristics of FHR Patterns
• The clinical application of electronic FHR
monitoring (EFM) consists of three
interdependent elements:
(1) Definition, that is, the words used to describe
the FHR observations;
(2) Interpretation, or the physiologic significance
of the FHR observations; and
(3) Management, or the clinical response to the
FHR observations.
The standardized NICHD definitions
Specific Fetal Heart Rate Patterns
 BASELINE RATE

• Baseline FHR is mean FHR rounded to

increments of 5 beats/min during a 10-
minutes segment excluding accelerations,
decelerations, and periods of marked
variability.
• A normal FHR baseline of 110 to 160
beats/min is consistent with normal
neurologic regulation of the FHR.
 Baseline FHR
• Fetal Tachycardia is defined as a baseline rate
above 160 beats/min for at least 10 minutes.

• Fetal Bradycardia is defined as a baseline rate

below 110 beats/min for at least 10 minutes.
Fetal Tachycardia
Fetal Bradycardia
 VARIABILITY
• Variability is fluctuations in the baseline FHR
that are irregular in amplitude and frequency.
• Variability is measured from the peak to the
trough of the fluctuations.
• Standardized NICHD nomenclature classifies
variability as absent, minimal, moderate, or
marked.
 Absent Variability

• Absent: when the amplitude range of the

FHR fluctuations is undetectable to the
unaided eye.
 Minimal Variability
• Minimal variability when the amplitude range
is visually detectable but is less than or equal
to 5 beats/min.
 Moderate Variability
• Moderate variability When the amplitude
range of the FHR fluctuations is 6 to 25
beats/min,
 Marked Variability
• Marked variability when the amplitude range
of the FHR fluctuations is greater than 25
beats/min.
 VARIABILITY Cont..
• The 2008 NICHD consensus report concluded
that moderate variability reliably predicts the
absence of fetal metabolic acidemia at the
time it is observed.
• However, the converse is not true; minimal or
absent variability does not confirm the
presence of fetal metabolic acidemia or
ongoing hypoxic injury.
 ACCELERATION
• Acceleration is as an abrupt increase (onset to
peak <30 seconds) in FHR above the baseline.
• The peak is at least 15 beats/min above the
baseline, and the acceleration lasts at least 15
seconds from the onset to return to baseline.
 ACCELERATION cont..
• Before 32 weeks of gestation, an acceleration
is defined as having a peak at least 10
beats/min above the baseline and a duration
of at least 10 seconds.
• An acceleration that lasts at least 2 minutes
but less than 10 minutes is defined as a
prolonged acceleration.
• An acceleration that lasts 10 minutes or longer
is defined as a baseline change.
 ACCELERATION cont..
• The 2008 NICHD consensus report concluded that
accelerations reliably predict the absence of fetal
metabolic acidemia at the time they are observed.
• However, the converse is not true.
• Accelerations can be provoked with a variety of
methods
• Accelerations provoked by external stimuli have
the same clinical significance as spontaneous
accelerations.
OTHER FACTORS THAT CAN INFLUENCE THE FHR TRACING BY MECHANISMS
NOT SPECIFICALLY RELATED TO FETAL OXYGENATION
 DECELERATIONS

• Decelerations in the FHR are categorized as

early, late, variable, or prolonged and are
quantitated by depth in beats per minute
below the baseline and duration in minutes
and seconds.
 EARLY DECELERATION
• Early deceleration is defined as a gradual
decrease (onset to nadir <30 seconds) in FHR
from the baseline and a subsequent return to
baseline associated with a uterine
contraction.
• In most cases the onset, nadir, and recovery of
the deceleration occur at the same time as the
beginning, peak, and end of the contraction,
respectively.
 Early deceleration Cont..

• Early decelerations are not associated with

interruption of fetal oxygenation or adverse
neonatal outcome and are considered
clinically benign.
 LATE DECELERATION
• Late deceleration of the FHR is defined as a
gradual decrease (onset to nadir ≥30 seconds)
of the FHR from the baseline and subsequent
return to the baseline associated with a
uterine contraction,
• In most cases the onset, nadir, and recovery of
the deceleration occur after the beginning,
peak, and ending of the contraction,
respectively.
 Late deceleration
• A Late deceleration is a reflex fetal response
to transient hypoxemia during a uterine
contraction.
• If interruption of fetal oxygenation is sufficient
to result in metabolic acidemia, a late
deceleration may result from direct hypoxic
myocardial depression during a contraction,
 VARIABLE DECELERATION
• Variable deceleration of the FHR is defined as
an abrupt decrease (onset to nadir <30
seconds) in FHR below the baseline.
• The decrease is at least 15 beats/min below
the baseline, the deceleration lasts at least 15
seconds, and fewer than 2 minutes pass from
onset to return to baseline.
• Variable decelerations can occur with or
without uterine contractions.
 Variable deceleration
• A variable deceleration represents a fetal
autonomic reflex response to transient
mechanical compression of the umbilical
cord.
 PROLONGED DECELERATION
• Prolonged deceleration of the FHR is defined
as a decrease, either gradual or abrupt, in FHR
at least 15 beats/min below the baseline that
lasts at least 2 minutes from onset to return to
baseline.
• A prolonged deceleration that lasts 10 minutes
or longer is defined as a baseline change.
 Prolonged deceleration
• A prolonged deceleration reflects interruption
of oxygen transfer from the environment to
the fetus at one or more points along the
oxygen pathway.
 SINUSOIDAL PATTERN
• The Sinusoidal pattern, is a smooth, sine
wave–like undulating pattern in FHR baseline
with a frequency of 3 to 5 cycles/min that
persists for at least 20 minutes.
• Although the pathophysiologic mechanism is
not known, this pattern is classically
associated with severe fetal anemia.
The Three-tier system
• When patterns are normal or “reassuring”
(category I),
– There is almost always normal oxygenation,
– the baby is born vigorous, with normal pH
and Apgar scores.
• However, when the pattern is non-reassuring
(categoryII),
– The baby is more often normal than
depressed or acidotic.
MANAGEMENT OF NRFHRPs
A Standardized “ABCD” Approach to FHR Management

• If assessment of the FHR indicates that the

tracing is not in category I, further evaluation
is warranted.
• A - Assess the Oxygen Pathway
• B- Begin Corrective Measures as Indicated
• C- Clear Obstacles to Rapid Delivery
• D- Determine Decision-to-Delivery Time
Assess the Oxygen Pathway
 CONSERVATIVE CORRECTIVE MEASURES

• SUPPLEMENTAL OXYGEN
• MATERNAL POSITION CHANGES
• INTRAVENOUS FLUID ADMINISTRATION
• CORRECT MATERNAL HYPOTENSION
• REDUCE UTERINE ACTIVITY
• AMNIOINFUSION
• ALTER SECOND-STAGE PUSHING AND
BREATHING TECHNIQUE
 Operative Intervention for NRFS
• Category I is strongly predictive of the
absence of hypoxia and normal fetal acid-base
status, and these patterns require no
intervention.
• Category III patterns are predictive of a fetal
metabolic acidosis and require “prompt
evaluation.” and immediate operative
delivery
• Category II includes more than 80% and
require evaluation, continued surveillance and
reevaluation based on circumstance
• The ACOG recommends that “all hospitals
have the capability of performing a C/D within
30min of the decision to operate,” but that
“not all indications for a C/D will require a
30min response time.”
Expectant Management Versus Delivery

Algorithm for management of category II fetal heart rate tracings.

Other Methods of Evaluating Fetal Status

• Intrapartum Fetal Scalp pH and Lactate

Determination
• Fetal Scalp Stimulation and Vibroacoustic
Stimulation
• Fetal Pulse Oximetry
 Auscultation as an Alternative

• Almost all RCT have demonstrated that

intermittent auscultation one-to-one is as
effective as EFM in detecting fetal hypoxia in
labor.
• Therefore, it is reasonable to conclude that
auscultation is an acceptable option for
monitoring the fetus in labor when certain
conditions are in place.
• The patient should have one-on-one nursing.
 SUMMARY
• The goal of intrapartum FHR monitoring is to assess the adequacy of fetal
oxygenation during labor so that timely and appropriate steps can be taken
when necessary to avoid fetal hypoxic injury.
• Fetal oxygenation involves the transfer of oxygen from the environment to the
fetus.
• The consequences of interruption of fetal oxygenation can lead sequentially to
fetal hypoxemia (low oxygen content in the blood), fetal hypoxia (low oxygen
content in the tissues), metabolic acidosis (accumulation of lactic acid in the
tissues), metabolic acidemia (accumulation of lactic acid in the blood), and
eventually injury or death.
• The FHR monitor provides reliable information regarding interruption of the
oxygen pathway.
• The negative predictive value of electronic FHR monitoring is excellent.
• A normal test virtually precludes fetal hypoxic injury at the time it is observed.
 SUMMARY
• The positive predictive value of electronic FHR monitoring is
poor.
• Abnormal FHR monitoring accurately predicts CP
approximately one time out of 500, yielding a false-positive
rate above 99%.
• No randomized controlled trials, cohort studies, case control
studies, or other peer-reviewed studies in the literature
support the hypothesis that fetal head compression caused by
uterine contractions or maternal pushing efforts can cause
local cerebral ischemia and hypoxic-ischemic injury in the
absence of the established mechanism of global hypoxia.
 Reference
• GABBE 7TH EDITION
• CREASY AND RESNIKS MFM 7TH EDITION
• WILLIAM OBSTETRIC 24TH EDITION
• CURRENT OBSTETRICS AND GYNECOLOGY 11TH EDITION
• PRACTICAL GUIDE TO HIGH-RISK PREGNANCY AND DELIVERY
3RD EDITION
• HIGH RISK PREGNANCY MANAGEMENT OPTIONS 4TH EDITION