Intrapartum Fetal Assessment

Intrapartum Fetal Assessment done to monitor fetal well being as labor

progresses

Techniques Fetal Heart Rate Monitoring

Done in 80-90% of intrapartum assessment Fetal Scalp Blood Sampling Fetal Scalp Stimulation Vibroacoustic Stimulation Fetal Pulse Oximetry Fetal Echocardiography Intrapartum Doppler Velocimetry 

Internal EFHRMFHR measured by attaching a bipolar

spiral electrode directly to the fetus Invasive(+) Ruptured BOW

Internal EFHRM

External EFHRMFHR is monitored by using external

detectors applied on the maternal abdominal wall

Ultrasound Doppler PrincipleUltrasonic waves undergo a shift in

frequency as they are reflected from the moving fetal heart valves and from pulsatile blood ejected during systole

External EFHRM

Fetal Heart Rate Patterns Baseline Fetal Heart Rate (120 – 160 bpm) Approximate mean rate rounded to increments of

5 beats/min during a 10 min tracing segment Minimum baseline duration must be at least 2

minutes Exclude period of marked FHR variability and

periodic or episodic changes (e.g acceleration or deceleration)

Fetal Heart Rate Patterns Fetal Bradycardia (<110 bpm) A rate between 110 – 119 bpm, in the absence of

other non-reassuring patterns is not usually a sign of fetal compromise (Young, et al 1976)

Etiologies: Heart block Head Compression in occiput posterior or

transverse position

Fetal Heart Rate Patterns Fetal Tachycardia (>160 bpm) In the presence of good variability, tachycardia is not a

sign of fetal distress Etiologies:

Maternal fever (most common) Fetal hypoxia Fetal HF Drugs (beta sympathomimetics) Rebound (transient) tachycardia ff a deceleration

accompanied by decreased variability

Baseline FHR Variability is an important index of cardiovascular function

and appears to be regulated largely by the autonomic nervous system

Irregular fluctuations in the baseline FHR Regulated largely by the autonomic nervous

system (sympathetic & parasympathetic “push-pull” mediated via the sinoatrial node, produces beat-to-beat oscillation of the baseline FHR)

2 Types of Variability Short- Term Variability reflects the instantaneous change in FHR from

one beat or R wave to the next measure of time interval between cardiac

systoles beat to beat changes

2 Types of Variability Long-Term Variability the oscillatory changes that occur during the

course of 1 minute and result in the waviness of the baseline

Normal frequency: 3-5 cycles/min

Grades of FluctuationAbsent variability

amplitude range undetectable; flat Ominous

Minimal <5 bpm secondary to fetal sleep or drugs

Moderate 6 to 25 bpm normal

Marked > 25 bpm

Variability persistently minimal or absent FHR variability

appears to be the most significant intrapartum sign of fetal compromise

During antepartum assessment, the indicator for fetal well-being are accelerations, here in intraprtum assessment, it is variability.

on the other hand, the presence of good FHR variability may not always be predictive of a good outcome

Etiologies Fetal metabolic acidosis CNS depressants (anesthesia, anti-seizure

drugs, etc) Fetal sleep cycles Congenital anomalies Prematurity Fetal tachy Pre-existing neurologic abnormality

Acceleration an abrupt increase in FHR above baseline with

onset to peak of the acceleration less than 30 sec and less than 2 min in duration

adequate accelerations are defined as: <32 wks ≥10 bpm above baseline for ≥10

sec >32wks ≥15 bpm above baseline for ≥ 15

sec

Deceleration an abrupt increase in FHR above baseline with

onset to peak of the acceleration less than 30 sec and less than 2 min in duration

adequate accelerations are defined as: <32 wks ≥10 bpm above baseline for ≥10

sec >32wks ≥15 bpm above baseline for ≥ 15

sec

3 Types of Deceleration Early decelerationsVariable decelerationsLate decelerations

3 Types of Deceleration Early decelerationsVariable decelerationsLate decelerations

Early Deceleration Gradual decrease in FHR with onset of deceleration to nadir in

≥ 30 sec Exact mirror image of uterine contraction Same timing with uterine contraction Gradual decline

The nadir occurs with the peak of a contraction head compression probably causes vagal nerve activation as

a result of dural stimulation and that mediates the heart rate deceleration

not associated with fetal hypoxia, acidemia or low APGAR scores

typically occur during the 2nd stage of labor

Late Deceleration Smooth and gradual decrease in FHR with onset of

deceleration to nadir ≥ 30 sec Onset of the deceleration occurs after the beginning of the

contraction, and the nadir of the deceleration occurs after the peak of the contraction

Etiologies: Excessive uterine contractions (hyperstimulation), maternal

hypotension (by epidural anesthesia) or maternal hypoxemia Reduced placental exchange/ placental dysfunction as in

hypertensive disorders, diabetes, collagen vascular disorders, IUGR, abruption

Uteroplacental insufficiency

Management of Late Deceleration place patient on side (left)

to release the pressure from the major vessel (aorta)

administer 02 by tight face mask or nasal prong discontinue oxytocin- you might have triggered

hyperstimulation correct any hypotension IV hydration if hyperstimulation is present, consider terbutaline

0.25 mg SC

Variable Deceleration from the most recently determined baseline rate the onset of deceleration to nadir is less than 30 sec the deceleration lasts ≥ 15 sec and < 2 minutes pure variables are uncommonly associated with adverse fetal outcome UMBILICAL CORD OCCLUSION (e.g. Nuchal cord or cord prolapse) Features: “shouldering” Initial shallow acceleration

due to occlusion of umbilical vein Sudden Deceleration

Umbilical artery Late acceleration

Compensatory increase in heart rate

Other Fetal Heart Rate Patterns

Saltatory Pattern also associated with cord compression marked variability consists of rapidly recurring couplets of

acceleration and deceleration causing relatively large oscillations of the baseline FHR

Lambda Pattern an acceleration followed by a variable

deceleration with no acceleration at the end of deceleration – no shouldering

not ominous seen in early labor may result from mild cord compression or stretch

Overshoot variable deceleration followed by prolonged

acceleration indicates an abnormal cord position

Prolonged Deceleration an isolated deceleration lasting for 2 min or longer

but less than 10 min from onset to return to baseline

Etiologies: cervical exam uterine hyperactivity cord entanglement maternal supine hypotension epidural anesthesia maternal valsalva

FHR Patters During the 2nd Stage of Labor

Deccelerations are virtually present most of the time during the 2nd stage of labor, with both cord compression and head compression implicated as causes

Abnormal baseline FHR- either bradycardia or tachycardia, absent beat-to-beat variability, or both- in the presence of 2nd stage deceleration is associated with increased fetal compromise

Fetal Scalp Blood Sampling

an intrapartum procedure for the evaluation of fetal acid base status

by determining the pH in capillary scalp blood, fetus in serious distress may be identified

procedure is now used uncommonly

Fetal Scalp Blood Sampling

this procedure is performed only in select cases of deliveries in which the FHR raise some concern regarding fetal status but not enough to mandate immediate delivery

pH of fetal capillary scalp blood is usually lower than that of umbilical venous blood and approaches that of umbilical artery

Fetal Scalp Blood Sampling

a confusing / non-reassuring FHR pattern is present (may be subjective: get the pH if the baby is acidotic or not)

variability ≤ 5 bpm with / without periodic changes or if absent variability

mixed deceleration pattern which complicates interpretation

Contraindications

mother known carrier of hemophilia and fetus either affected or of unknown status

mother is HIV seropositive active maternal genital infection e.g. herpes

Interpretation> 7.25 labor is observed, repeat FSBS every

2-3 hours

7.20 – 7.25

repeat FSBS within 30 min

< 7.20 repeat FSBS immediately while preparing for surgery, if confirmed, delivery is indicated.

Procedure An illuminated endoscope is inserted through the dilated

cervix after ruptured membranes so as to press firmly against fetal scalp

The skin is wiped clean with a cotton swab and coated with a silicone gel to cause the blood to accumulate as discrete globules

An incision is made through the skin to a depth of 2 mm with a special blade on a long handle

As a drop of blood forms on the surface, it is immediately collected into a heparinized glass capillary tube

pH of blood is measured promptly

Fetal Scalp Stimulation

Clark, 1984 acceleration of FHR in response to pinching with

an Allis clamp was associated with normal pH however, failure to provoke acceleration was not

uniformly predictive of fetal acidemia

Fetal Scalp Stimulation

Elimian, 1997 presence of acceleration following the gentle

digital stroking revealed scalp pH ≥ 7.20 without acceleration, however, only 30% has a

scalp pH <7.20

Vibroacoustic Stimulation

use of sound to stimulate/startle the baby involves the use of an electronic artificial larynx

(or a bell) placed a cm or so from or directly onto the maternal abdomen

response is considered normal if FHR acceleration occurs within 15 sec after stimulation and with prolonged fetal movements

effective predictor of fetal acidosis in the setting of variable decelerations

Fetal Pulse Oximetry

a unique pad-like sensor is inserted through the cervix and positioned against the fetal face, where it is held by the uterine wall

the lower limit for normal fetal oxygen saturation is 30%

saturation values below 30%, when persistent for 2 min or longer, are associated with an increased risk of potential fetal compromise

Fetal Electrocardiography

Involves ST segment of the fetal ECG is analyzed, because changes occurs as fetal hypoxia worsens

Techniques requires internal monitoring of the FHR and a special equipment to process the fetal ECG

ST abnormalities may occur late in the course of fetal jeopardy

Intrapartum Doppler Velocimetry

Doppler analysis of the umbilical artery Ultrasound needs to be done in order to locate

umbilical artery Poor predictor of adverse perinatal outcomes Little role in the surveillance of fetal well-being

during labor; rarely done

Fetal Distress

Reassuring FHR pattern – suggests a restoration of confidence by a particular pattern

Non-reassuring FHR pattern – suggests inability to remove doubt

NICHD Research Planning Workshop (2008) FHR PatternsPattern Workshop InterpretationsCategory I:NORMAL

Baseline: 110 – 160 bpm (120 in the book)Variability: 6 – 25 bpm (moderate)Accelerations: Present or AbsentLate or Variable Decelerations: AbsentEarly Decelerations: Present or Absent

Category II:INDETERMINATE

Include all FHR tracings not categorized as Category I or III

Category III:ABNORMAL-non-reassuring

Include either:- Absent Baseline FHR variability and any of the following: Recurrent late decelerations Recurrent variable decelerations Shift of baseline to bradycardia- Sinusoidal Pattern

Meconium in the Amniotic Fluid

Obstetrical teaching throughout the past century has included the concept that meconium passage is a potential warning of fetal asphyxia

Not necessarily a warning that the fetus is asphyxiated Nathan, 1994 – Meconium is a “low-risk obstetrical

hazard” - perinatal mortality attributed to meconium was 1 death per 1000 live births

Meconium passage is a result of relaxation of the sphincter ani muscle induced by faulty aeration of fetal blood

Theories of Fetal Passage of Meconium

Fetuses pass meconium in response to hypoxia and that meconium therefore signals fetal compromise (Walker, 1953)

In utero passage of meconium may represent normal gastrointestinal tract maturation under neural control (Matthews & Warsaw, 1979)

Could follow vagal stimulation from a common but transient umbilical cord entrapment ad resultant increased peristalsis, thus fetal release of meconium also could represent physiological process (Hon, 1961)

Meconium Aspiration Syndrome

was significantly associated with fetal acidemia at birth

Other significant correlates of aspiration: CS forceps to expedite delivery intrapartum heart rate abnormalities depressed APGAR score need for assisted ventilation at delivery

Meconium Aspiration Syndrome

Meconium in amniotic fluid is a fetal environmental hazard (when acidemia supervenes) rather than a marker of a preexistent compromise.

Fetal hypercarbia/acidemia → stimulates fetal respiration → aspiration of meconium, into the alveoli → lung parenchymal injury (Ramin, 1996)

Management Options of Fetal Distress

1. Tocolysis Terbutaline sulfate 1.25 mg IV or SQ single dose –

uterine relaxant Temporizing maneuver to relax the uterus and

improve fetal oxygenation, prior to CS

Management Options of Fetal Distress

2. Amnioinfusion (transvaginal) For oligohydramnios For meconium stained amniotic fluid 500-800 ml bolus of warmed normal saline

followed by a continuous infusion of approximately 3 ml per min

Intrapartum Surveillance of Uterine Activity

Internal Uterine Pressure Monitoring Contractions occurring within 3 minutes, whether mild,

moderate or strong, you should record it. amniotic fluid pressure is measured between and during

contractions by a fluid-filled plastic catheter with its distal tip located above the presenting part

the catheter is connected to a strain-gauge pressure sensor adjusted to the same level as the catheter tip in the uterus

the amplified electrical signal produced in the strain gauge is recorded on a calibrated moving paper strip simultaneously with the fetal heart rate recording

External Monitoring

uterine contractions can be monitored by a displacement transducer in which the transducer button or plunger is held against the abdominal wall (at the fundus)

it does not give an accurate measure of intensity but only the relative intensity (not as accurate as putting a catheter inside the uterine cavity above the presenting part)

but can give a good indication of the onset, peak and end of contraction

Montivideo Units

Used to measure the units of uterine contraction during labor

Direct measure of the pressure of uterine contractions

Uterine performance is the product of the intensity of a contraction in mmHg x contraction frequency per 10 min

Get the amplitude x 3 u.c./10min

Montivideo Units

Labor usually commences when uterine activity reaches values between 80 & 120 Montevideo units (~3 contractions / 10 min with an intensity of 40 mmHg)

No clear cut division

Montivideo Units

First stage of labor Intensity: 25-50 mmHg Frequency: 3-5 u.c. / 10 min

Second stage (full dilatation) Intensity: 80-100 mmHg Frequency: 5-6 u.c. / 10 min (every 2 minutes)  Duration: 60-80 sec, constant from 1st stage to 2nd stage 

Origin and Propagation of Contractions10 mmHg palpable contractions

<40 mmHg uterine wall can be readily depressed (mild to moderate)

>40 mmHg Uterine wall can no longer be readily depressed/indented (contraction is at its peak)

>15 mmHg pain can be appreciated, the minimum pressure required for distending the lower uterine segment and cervix

Origin and Propagation of Contractions

the normal contraction wave of labor originates near the uterine end of one of the fallopian tubes - “pacemakers”

the right pacemaker dominates over the left and starts the great majority of contractile waves

contractions spread from the pacemaker area throughout the uterus at 2 cm/sec, depolarizing the whole uterus within 15 sec

the depolarizing wave propagates downward toward the cervix

Summary

FHR patterns that you should be able to determine in a strip: Baseline FHR

2 mins Without any accelerations or decelerations N: 120-160 Bradycardia: <110 Tachycardia:> 160

Summary

Variability Absent Minimal: <5 Normal: 6-25 Marked: >25

Uterine hyperstimulation

Summary

Accelerations <32 wks ≥10 bpm above baseline for ≥10 sec >32wks ≥15 bpm above baseline for ≥ 15 sec

Summary

Decelerations Episodic

unrelated to uterine contractions Periodic

associated with uterine contractions

Summary

Early associated with head compression; lowest FHR corresponds with peak of uterine contraction,

creating a mirror-imag not associated with fetal hypoxia, acidemia, low APGAR

Summary

Late uteroplacental insufficiency lowest heartbeat occurs after the peak of uterine

contraction fetal hypoxia

Summary

Variable cord compression uncommonly associated with adverse fetal outcome, unless

with pathologic features sharp (compared to the others, which are gradual) decrease

in fetal heartbeat unrelated to uterine contraction

Summary

Fetal scalp blood sampling: N: >7.25 < 7.20 – acidosis is suspected

Scalp stimulation and vibroacoustic stimulation should cause FHR acceleration

Pulse oximetry: N: 30% O2 sat

Summary

Meconium staining: May be pathologic, but most of the time

physiologic Watch for occurrence of meconium aspiration

acute or unpredictable check the fetal vocal cords if there is meconium - if

none, baby is ok; if meconium-stained, suspect meconium- aspiration

Summary

Amnioinfusion To correct oligohydramnios, thus improving FHR

pattern Not recommended in meconium-stained

amniotic fluid because you may be increasing the environmental hazard characteristic of the meconium, which may cause meconium aspiration

Summary

Montevideo unit Uterine pressure x # of contraction/ 10 min

Uterine pacemaker near the uterine end of the fallopian tube right dominating the left propagate at 2 cm/s towards the cervix

Electronic Fetal HR Monitoring Internal EFHRM External EFHRM