Physiologic Basis for Fetal Heart Rate Monitoring

Physiologic Basis for Fetal Heart Rate Monitoring

The objective of intrapartum fetal heart rate (FHR)
monitoring is to prevent fetal injury that might result
from interruption of fetal oxygenation during labor
The underlying assumption is that the FHR tracing can
reveal specific information regarding fetal
oxygenation
Understanding the physiologic basis for electronic
FHR monitoring requires a realistic appraisal of this
basic assumption

Goal of Fetal Heart Rate Monitoring

Intrapartum fetal heart rate monitoring is intended to
assess the adequacy of fetal oxygenation during labor
Fetal oxygenation involves:
The transfer of oxygen from the environment to the fetus
The fetal response to interrupted oxygen transfer
Certain FHR patterns provide reliable information
regarding both of the basic elements of fetal
oxygenation

Transfer of Oxygen from The Environment To The Fetus

Oxygen is carried from the environment to the fetus by
maternal and fetal blood along a pathway that includes
the maternal lungs, heart, vasculature, uterus, placenta
and umbilical cord.
Environment

Lungs

The Oxygen Pathway

Heart

Vasculature

Uterus

Placenta

Umbilical cord

Fetus

Maternal Lungs
Inspiration carries oxygen from the external
environment to the distal air sacs of the lung, the
alveoli
Interruption of oxygen transfer from the environment
to the alveoli can result from airway obstruction (for
example asthma) or from interruption of breathing
caused by depression of central respiratory control
(narcotics, magnesium sulfate, seizure)

Maternal Lungs
From the alveoli, oxygen diffuses across a thin
barrier into the pulmonary capillary blood
Interruption of oxygen transfer from the alveoli to
the pulmonary capillary blood can be caused by
factors such as ventilation-perfusion mismatch
and diffusion defects (such as pneumonia or
pulmonary embolus)

Interruption of oxygen transfer at the level of the lungs

In an obstetric population, pulmonary causes of
interrupted oxygenation include:
Respiratory depression
Medications
Seizure
CNS depression
Pulmonary embolus, amniotic fluid embolus
Pulmonary edema
Pneumonia, adult respiratory distress syndrome
Asthma,atelectasis

Maternal blood
After diffusing from the pulmonary alveoli into maternal
blood, more than 98% of oxygen combines with
hemoglobin in maternal red blood cells
Approximately 1-2% remains dissolved in the blood and is
measured by the partial pressure of dissolved oxygen
(PaO2)
A normal adult PaO2 value of 95-100 mmHg results in
hemoglobin saturation of approximately 95-98%,
indicating that hemoglobin is carrying 95-98% of the
total amount of oxygen it is capable of carrying

Interruption of oxygen transfer at the level of the

maternal blood
Interruption of oxygen transfer from the environment to
the fetus due to abnormal maternal oxygen carrying
capacity can result from severe anemia or from
hereditary or acquired abnormalities affecting oxygen
binding (hemoglobinopathies, methemoglobinemia)
In an obstetric population, reduced maternal oxygen
carrying capacity rarely causes acute interruption of
fetal oxygenation

Maternal heart
From the lungs, pulmonary veins carry oxygenated
maternal blood to the heart
Blood enters the left atrium with a PaO2 of
approximately 95-100 mmHg
Oxygenated blood passes from the left atrium, through
the mitral valve into the left ventricle and out the
aorta for systemic distribution

Interruption of oxygen transfer at the level of the heart

Interruption of oxygen transfer from the environment to the
fetus at the level of the maternal heart can be caused by
any condition that reduces cardiac output, including:
Altered heart rate (arrhythmia)
Reduced preload (hypovolemia, compression of the IVC)
Impaired contractility (ischemic heart disease,
cardiomyopathy)
Increased afterload (hypertension)

Interruption of oxygen transfer at the level of the heart

In addition, structural abnormalities of the heart and/or
great vessels may impede the normal ability to
pump blood (valvular stenosis, valvular insufficiency,
pulmonary hypertension, coarctation of the aorta)
In a healthy obstetric patient, the most common cause
of reduced cardiac output is reduced preload
(hypovolemia, compression of the inferior vena
cava).

Maternal vasculature
Oxygenated blood leaving the heart is carried by the
systemic vasculature to the uterus
The path includes the aorta, iliac vessels and the uterine
arteries
From the uterine artery, oxygenated blood travels
through the arcuate arteries, the radial arteries and
finally the spiral arteries before exiting the maternal
vasculature and entering the intervillous space of the
placenta

Interruption of oxygen transfer at the level of the maternal

vasculature
Hypotension
Regional anesthesia
Hypovolemia (dehydration, hemorrhage)
Impaired venous return
Impaired cardiac output
Medications
Vasoconstriction of distal arterioles in response to
endogenous vasoconstrictors or medications

Uterus
Between the maternal uterine arteries and the
intervillous space of the placenta, the arcuate, radial
and spiral arteries traverse the muscular wall of the
uterus

Interruption of oxygen transfer at the level of the uterus

Interruption of normal oxygen transfer from the
environment to the fetus at the level of the uterus
commonly results from uterine contractions that
compress intramural blood vessels and impede the flow
of oxygenated maternal blood into and out of the
intervillous space
Less common causes include uterine rupture or trauma
The evaluation of uterine activity is reviewed in a separate
module

Placenta
The placenta is the maternal-fetal interface that
facilitates the exchange of gases, nutrients, wastes
and other molecules (for example antibodies,
hormones, medications) between maternal blood in
the intervillous space of the placenta and fetal blood
in the villous capillaries

Placental causes of interrupted oxygenation

Many conditions can interfere with the normal transfer
of oxygen across the placenta
Clinically, the most common cause of acute
interruption of oxygen transfer at level of the
placenta is separation of the placenta from the
uterine wall (abruption, bleeding placenta previa)
Fetal-maternal hemorrhage and vasa previa should be
considered in the appropriate clinical setting

Fetal blood
After oxygen has diffused from the intervillous space
across the placental blood-blood barrier and into
fetal blood, the PaO2 in the umbilical vein returning
to the fetus is in the range of 35 mmHg and fetal
hemoglobin saturation is between 50 and 70%

Umbilical cord
After oxygen combines with fetal hemoglobin in the villous
capillaries, oxygenated blood returns to the fetus by
way of a single umbilical vein within the umbilical cord
Interruption of the normal transfer of oxygen from the
environment to the fetus at the level of the umbilical
cord most often results from mechanical cord
compression
Other uncommon causes may include vasospasm,
thrombosis, atherosis, hypertrophy, hemorrhage,
inflammation or a true knot.

Summary
Oxygen Pathway

Some causes of interrupted oxygen transfer

Lungs

Respiratory depression (narcotics, magnesium)

Apnea, seizure (eclampsia)
Pulmonary embolus, pulmonary edema
Pneumonia/ARDS
Asthma, atelectasis

Heart

Reduced cardiac output

Hypovolemia
Compression of the inferior vena cava
Regional anesthesia (sympathetic blockade)
Cardiac arrhythmia

Vasculature

Hypotension
Hypovolemia
Compression of the inferior vena cava
Regional anesthesia (sympathetic blockade)
Medications (hydralazine, labetalol, nifedipine)

Uterus

Excessive uterine activity

Uterine stimulants (prostaglandins, oxytocin)
Uterine rupture

Placenta

Placental separation
Rarely vasa previa
Rarely fetal-maternal hemorrhage
Placental infarction, infection (usually confirmed retrospectively)

Umbilical cord

Cord compression
Cord prolapse, true knot

Fetal oxygenation
Oxygen transfer from the environment to the fetus
represents the first component of fetal oxygenation
The second component of fetal oxygenation involves
the fetal physiologic response to interrupted oxygen
transfer.

Fetal response to interrupted oxygen transfer

Depending upon frequency and duration, interruption
of oxygen transfer at any point along the oxygen
pathway may result in progressive deterioration of
fetal oxygenation
The cascade begins with hypoxemia, defined as
decreased oxygen content in the blood
At term, hypoxemia is characterized by an umbilical
artery PaO2 below the normal range of 15-25
mmHg

Fetal response to interrupted oxygen transfer

Recurrent or sustained hypoxemia can lead to
decreased delivery of oxygen to the tissues and
reduced tissue oxygen content, or hypoxia
Normal homeostasis requires an adequate supply of
oxygen and fuel in order to generate the energy
required by basic cellular activities

Fetal response to interrupted oxygen transfer

When oxygen is readily available, aerobic metabolism
generates energy efficiengly in the form of ATP
By-products of aerobic metabolism include carbon
dioxide and water
When oxygen is in short supply, tissues may be forced
to convert from aerobic to anaerobic metabolism,
generating energy less efficiently and resulting in
the production of lactic acid

Fetal response to interrupted oxygen transfer

Accumulation of lactic acid in the tissues results in
metabolic acidosis
Lactic acid accumulation can lead to utilization of
protective buffer bases (primarily bicarbonate) to help
stabilize tissue pH
If the buffering capacity is exceeded, the blood pH may
begin to fall, leading to metabolic acidemia
It is critical to distinguish between metabolic acidemia and
and respiratory acidemia

Fetal response to interrupted oxygen transfer

Metabolic acidemia is caused by accumulation of lactic
acid in the setting of anaerobic metabolism
Respiratory acidemia is caused by accumulation of
CO2, a by product of aerobic metabolism that than
increase in the blood when placental gas exchange is
suboptimal
In contrast to metabolic acidemia, isolated respiratory
acidemia has no know association with adverse
outcome

Fetal response to interrupted oxygen transfer

Regardless of the specific cause of interrupted fetal
oxygenation, recurrent or sustained tissue hypoxia and
acidosis can lead to loss of peripheral vascular smooth
muscle contraction, reduced peripheral vascular
resistance and hypotension

Fetal response to interrupted oxygen transfer

If interrupted oxygen transfer progresses to the stage of
metabolic acidemia and hypotension, multiple organs
and systems (including the brain and heart) can suffer
hypoperfusion, reduced oxygenation, lowered pH and
reduced delivery of fuel for metabolism
Interruption of normal cellular metabolism can to lead to
cellular dysfunction, tissue dysfunction and even death

Injury threshold
We have reviewed fetal oxygenation in detail, including
each step of oxygen transfer from the environment to
the fetus and each stage of the fetal physiologic
response to interrupted oxygenation
We have reviewed the mechanisms of injury in the
setting of recurrent or sustained interruption of
oxygenation
The precise relationship between interrupted fetal
oxygenation and neurologic injury is complex and
incompletely understood

Injury threshold
Electronic FHR monitoring was introduced with the
expectation that it would significantly reduce the incidence
of neurologic injury (specifically cerebral palsy) caused by
intrapartum interruption of fetal oxygenation
In recent years, it has become apparent that most cases of
cerebral palsy are unrelated to intrapartum events and
therefore cannot be prevented by intrapartum FHR
monitoring
Nevertheless, a significant minority of such cases may be
related to intrapartum events and might be preventable

Injury threshold
In 1999, the International Cerebral Palsy Task Force
published a consensus report regarding the relationship
between intrapartum interruption of fetal oxygenation
and subsequent neurologic injury
In January, 2003, ACOG and the American Academy of
Pediatrics jointly published a monograph entitled
Neonatal Encephalopathy and Cerebral Palsy: Defining
the Pathogenesis and Pathophysiology summarizing the
world literature regarding the relationship between
intrapartum events and neurologic injury

Injury threshold
Agencies and professional organizations that reviewed
and endorsed the ACOG-AAP report include:
American College of Obstetricians and Gynecologists
American Academy of Pediatrics
Centers for Disease Control
The Child Neurology Society
March of Dimes Birth Defects Foundation
National Institute of Child Health and Human Development
Royal Australian and New Zealand College of Obstetricians and
Gynecologists
Society for Maternal-Fetal Medicine
Society of Obstetricians and Gynaecologists of Canada

Injury threshold
The consensus report established four essential
criteria defining an acute intrapartum event sufficient
to cause cerebral

Essential criteria that define an acute intrapartum event

sufficient to cause cerebral palsy (must meet all four)
1. Umbilical cord arterial blood pH < 7 and base deficit 12
mmol/L
2. Early onset of severe or moderate neonatal encephalopathy in
infants born at 34 or more weeks of gestation
3. Cerebral palsy of the spastic quadriplegic or dyskinetic type
4. Exclusion of other identifiable etiologies such as trauma,
coagulation disorders, infectious conditions or genetic
disorders

Essential criteria that define an acute intrapartum event

sufficient to cause cerebral palsy
The first criterion indicates that intrapartum interruption of
fetal oxygenation does not result in neurologic injury
unless it progresses at least to the stage of significant
metabolic acidemia (umbilical artery pH < 7 and base
deficit 12 mmol/L)
It is important to note that fetal injury is uncommon even
when metabolic acidemia is present
It is also important to understand that respiratory acidemia
is not a recognized risk factor for fetal injury

Essential criteria that define an acute intrapartum event

sufficient to cause cerebral palsy
The second criterion highlights an equally important point:
intrapartum interruption of fetal oxygenation does not
result in cerebral palsy without first causing moderatesevere neonatal encephalopathy
The report further clarified that neonatal encephalopathy
has many possible causes. Hypoxic-ischemic
encephalopathy resulting from intrapartum interruption
of fetal oxygenation represents only a small subset of
the larger category of neonatal encephalopathy

Essential criteria that define an acute intrapartum

event sufficient to cause cerebral palsy
The third criterion emphasizes that different subtypes
of cerebral palsy have different clinical origins
Spastic quadriplegia is associated with injury to the
parasaggital cerebral cortex and involves abnormal
motor control of all four extremities
The dyskinetic subtype of cerebral palsy is associated
with injury to the basal ganglia and involves
disorganized, choreoathetoid movements

Essential criteria that define an acute intrapartum event

sufficient to cause cerebral palsy
The report concluded that these are the only two subtypes
of cerebral palsy associated with term hypoxic-ischemic
injury
Specifically, spastic diplegia, hemiplegia, ataxia and
hemiparetic cerebral palsy are unlikely to result from
acute intrapartum hypoxia

Essential criteria that define an acute intrapartum event

sufficient to cause cerebral palsy
The report further concluded that other conditions,
including epilepsy, mental retardation and attention
deficit hyperactivity disorder do not result from birth
asphyxia in the absence of cerebral palsy

Essential criteria that define an acute intrapartum event

sufficient to cause cerebral palsy
The fourth criterion emphasizes that intrapartum hypoxicischemic injury is a potential factor in only a small
subset of all cases of cerebral palsy
Most cases of cerebral palsy are unrelated to intrapartum
events
The report identified four additional criteria that can help
establish the timing of injury, emphasizing that these
criteria are nonspecific to asphyxial insults

Criteria that collectively suggest the event occurred within

48 hours of birth
1. A sentinel hypoxic event immediately before or during labor
2. A sudden and sustained fetal bradycardia or the absence of FHR
variability in the presence of persistent late or variable
decelerations, usually after a hypoxic sentinel event when the
pattern was previously normal
3. Apgar scores of 03 beyond 5 minutes
4. Onset of multisystem involvement within 72 hours of birth

Summary
The physiology of fetal oxygenation involves the
sequential transfer of oxygen from the environment
to the fetus and the subsequent fetal response if
oxygen transfer is interrupted
Interruption of normal oxygen transfer can occur at
any point along the oxygen pathway
Recurrent or sustained interruption of normal oxygen
transfer can lead to progressive deterioration of fetal
oxygenation and eventually to potential fetal injury

Summary
However, significant metabolic acidemia (umbilical
artery pH < 7.0 and base deficit 12 mmol/L) has
been identified as an essential pre-condition to
intrapartum hypoxic injury
With respect to the relationship between fetal
oxygenation and potential injury, there is consensus
in the literature that interrupted oxygenation does
not result in fetal injury unless it progresses at least
to the stage of significant metabolic acidemia.

Summary
The physiologic basis of FHR monitoring can be
summarized in a few key concepts
The objective of intrapartum FHR monitoring is to
assess fetal oxygenation during labor
Fetal oxygenation involves the transfer of oxygen from
the environment to the fetus and the subsequent
fetal response if oxygen transfer is interrupted

Summary
Oxygen is transferred from the environment to the fetus by
maternal and fetal blood along a pathway that includes
the maternal lungs, heart, vasculature, uterus, placenta
and umbilical cord
Environment

Lungs

Heart

Vasculature

Uterus

Placenta

Umbilical cord

Fetus

Summary
The fetal response to interrupted oxygen transfer involves
a sequential physiologic progression:
Hypoxemia
Hypoxia
Metabolic acidosis
Metabolic acidemia

Fetal injury due to interrupted oxygenation does not occur

unless this process has progressed at least to the stage
of significant metabolic acidemia (umbilical artery pH
<7.0 and base deficit > 12 mmol/L)