INTRAPARTUM FETAL MONITORING

PRESENTOR : DR RIA M MODERATOR : DR LATIKA CHAWLA

SR MODERATOR : DR ANOOSHA RAVI
Electronic fetal monitoring

 Conitinuous EFM was introduced in 1960s.

 accurate information
 value in diagnosing fetal distress
 morbidity and fetal deaths
 superior to intermittent methods
 Electronic fetal monitoring

Indirect/External Direct/internal
 Direct/ internal

 Bipolar spiral electrode.

 Wire electrode penetrate fetal scalp.
 Second pole is a metal wing on electrode.
 Vaginal fluid create a saline electrical bridge that completes the
circuit.
 Reference electrode on maternal thigh
- eliminate electrical interferences
- 2 wires of bipolar electrode are attached to this.
• Electrical fetal cardiac signals P, QRS, T are amplified by feeding into cardiotachometer for
HR calculation.
• Most reliably detected : peak R wave voltage.
• (t) : time in milli sec between fetal R wave fed into cardiotachometer to calculate HR
• when a new R wave arrive a new HR is calculated.
• This phenomenon of continuous R-R wave fetal HR computation is known as BEAT – TO –
BEAT VARIABILITY.
• Also detect electrical cardiac complexes generated by mother.

• Maternal ECG signal is 5 times stronger than fetal.

• But amplitude is diminished than fetal when recorded through fetal scalp electrode.

• In LIVE fetus : maternal ECG is recorded but masked by fetal.

• In DEAD fetus : weak maternal ECG is amplified and shown as fetal HR.

• SPIKING : when fetus experience PAC, cardiotachometer seeks new HR rapidly and eratically causing spiking in

standard fetal monitor tracing.

Indirect/external

 Membrane rupture can be avoided

 Less precise
 ULTRASOUND DOPPLER PRINCIPLE is used to detect fetal HR.
 US waves undergo shift in frequency when reflected from moving heart valves and from
pulsatile blood ejected during systole.
 TRANSDUCER : emit US on maternal abdomen, when FHR is best detected.
 SENSOR : detect shift in frequency of reflected sound.
 Coupling gel is used as it conducts US poorly.
• AUTOCORRELATION : reflected US signal from moving fetal heart valves are analysed through a

microprocessor.

• Microprocessor compares incoming signal with most recent previous signal.

• US doppler signals are electronically edited before FHR data printed onto monitor paper.

• This is based on that FHR has regularity whereas NOISE is random without regularity.
Fetal heart rate pattern

 NICHD research planning workshop, proposed definitions for intrapartum of FHR pattern
during labour.
 SCALING : vertical 1 cm – 30 bpm(30-240 bpm)
paper speed : 3 cm/min
 Rate
 Beat to beat variability
 Fetal arrythmia
 Distinct patterns : sinusoidal/ saltatory
 Rate

 Baseline FHR : approximate mean rate rounded to increment of 5 bpm during a 10 min
tracing segment.
In 10 minutes tracing window the minimum interpretable baseline duration
must be atleast 2 minutes.
 Average FHR is considered as a result of tonic balance between accelerator(sympathetic
system) and decelerator(parasympathetic via vagus)on pacemaker cells.
 HR is also under control of arterial chemoreceptors(modulated by hypoxia and
hypercapnia)
 With increasing fetal maturation, HR decreases

 Continues postnatally

 By 8 years average rate is 90 bpm

 Baseline FHR decreases by approximately 1 b/m/week.

 This is corresponding to maturation of parasympathetic(vagal)heart control.

 WANDERING BASELINE :baseline is unsteady between 120-160bmp. It is suggestive of neurologically

unstable fetus. It may occur as a preterminal event
Bradycardia

 Baseline FHR < 110 bpm.

 In third trimester, baseline FHR 120-160
 110-119 in absence of other changes is not considered to represent fetal compromise.
 In 2nd stage of labour – low but normal HR – head compression – occipito
posterior/transverse.
 2% pregnancies – mild bradycardia observed with average 50 min duration.
 80-120 bpm with good variability is reassuring
 < 80 bpm – non reassuring
 Causes of fetal bradycardia

 Congenital heart block

 Fetal compromise
 Maternal hypothermia(under GA) sustained fetal bradycarida
 Severe pyelonephritis (not harmed by several hours of such
bradycardia)
 Tachycardia

 Baseline HR > 160 bpm

 Cause :
1. Maternal fever from chorioamnionitis ; typically is not associated with fetal compromise when these are
- associated periodic HR changes
- fetal sepsis
2. Fetal compromise() associated with concomitant HR deccelerations.
3.Cardiac arrythmias
4.Maternal administration of parasympathetic(atropine)/sympathetic
drugs(terbutaline)
Beat to beat variability

 Important index of cardiovascular function

 Regulated by ANS

 Sympathetic and parasympathetic “ push and pull’ mediated via SA node produces
moment to moment / beat to beat oscillations of HR.

 Normal 6-25 bpm,

 Such HR change is defined as baseline variability.

SHORT TERM
LONG TERM
 Instantaneous change in FHR from one beat to next
 Oscillatory changes during 1 minute
beat or R wave to next R wave.
 Results in waviness of baseline
 Measure of time interval between cardiac systoles.
 3-5 cycles/minute
 When ecg are measured directly with scalp
electrodes.
Increased variability

 Fetal breathing
short term variability-respiratory sinus arrythmia
 Fetal body movement
 Advancing gestation
upto 30 week rest = activity
> 30 week fetal inactivity - diminished variability
fetal activity – increased activity
 Gender doesnot affect variability
 As rate increases, baseline FHR become more physiologically fixed(less variable)
 As rate decreases, there is more variability.
 Decreased variability

 Fetal acidemia
 Severe maternal academia(DKA)
 Administration of analgesics drug labour
 CNS depressant drugs(narcotics,barbiturates,phenothiazines,tranquilizers and GA)
 MgSO4
 Decreased variability in absence of decelerations is unlikely to be due to fetal hypoxia.
Absent variability

 Persistent flat fetal HR baseline

 If within the normal baseline rate range and without deceleration – previous insult to fetus
that has resulted in neurological damage.
CARDIAC ARRHYTHMIA

 Findings can be bradycardia

tachycardia
abrupt baseline spiking
 Congenital heart block : intermittent baseline bradycardia
 Complete AV block is associated with maternal CT disease
 Arrhythmia can be documented when scalp electrodes are used.
 Supraventricular arrhythmias : considered little significant when there is coexistent – heart
failure evidenced by fetal hydrops
 Many SVT disappear in immediate neonatal period
Sinusoidal heart rate

 Fetal intra cranial hemorrhage

 Severe fetal asphyxia
 Severe fetal anemia from Rh alloimmunisation
 Fetomaternal hemorrhage
 Twin to twin transfusion syndrome
 Vasa previa with bleeding
 Chorioamnionitis
 Fetal distress
 Umbilical cord occlusion

 Following administration of Meperidine, Morphine , Alphaprodine,Butorphanol

--- due to narcosis : sine frequency of 6 cycles per minute
 Modanlou & Freeman
1. Stable baseline HR of 120-160 bpm with regular oscillations
2. Amplitude of 5-15 bpm
3. Longterm variability frequency of 2-5 cycles per minute
4. Fixed or flat short term variability
5. Oscillation of the sinusoidal waveform above or below a baseline
6. Absent accelerations
 MILD : amplitude 5-15 bpm
 INTERMEDIATE : 16-24 bpm
 MAJOR : >25 bpm

Pseudo sinusoidal pattern

Sine wave like baseline variation with periods of acceleration
Mild pseudo sinusoidal : epidural analgesia , meperidine
Intermediate pseudo sinusoidal : transient episodes of fetal hypoxia related to umbilical cord compression ,
fetal sucking
Pathophysiology :related to waves of arterial blood pressure , reflecting oscillations in the baroreceptor –
chemoreceptor feedback mechanism for control of the circulation
PERIODIC FETAL HEART RATE
CHANGES

 Deviations from baseline that are temporally related to uterine contractions

ACCELERATIONS
• A visually apparent abrupt increase in the FHR ( onset to peak in < 30 sec)
• At 32 weeks and beyond , an acceleration has a peak of 15 bpm or more above baseline , with a
duration of 15 sec or more but less tha 2 min from onset to return
•

• Before 32 weeks , an acceleration has a peak of 10 bpm or more above basdeline , with aduration od
>/= 10 sec but <2min from onset to return
 Fetal movement
 Stimulation by uterine contraction
 Umbilical cord occlusion
 Fetal stimulation during pelvic examination
 Fetal scalp blood sampling
 Vibro- acoustic stimulation
Represent intact neurohormonal cardiovascular control mechanism
Prolonged acceleration : >/= 2 min but < 10 min
If acceleration last > 10 min it is a baseline change
 EARLY DECELERATION
• Visually apparent usually symmetrical gradual decrease and return of the FHR associated with a uterine
contraction
• a gradual FHR decrease is defined as from the onset to the FHR nadir of >/= 30 sec
• Decrease in FHR is calculated from the onset to the nadir of the deceleration
• Nadir of the deceleration occurs at the same time as the peak of contraction
• In most cases the onset , nadir , and recovery of the deceleration are coincident with beginning , peak and
ending of contraction , respectively
Not associated with academia , hypoxia or low APGAR score
Head compression  dural stimulation  vagal nerve activation  deceleration
 LATE DECELERATION
• Visually apparent usually symmetrical gradual decrease and return of the FHR associated with a
uterine contraction
• a gradual FHR decrease is defined as from the onset to the FHR nadir of >/= 30 sec
• Decrease in FHR is calculated from the onset to the nadir of the deceleration
• 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
 Magnitude of late deceleration is seldom more than 30-40 bpm below baseline
 Not accompanied by acceleration s

 Maternal hypotension
 Excessive uterine activity
 Placental dysfunction
Interval or lag from the contraction onset until the late deceleration onset is directly related
to basal fetal oxygenation
 VARIABLE DECELERATION
• Visually apparent abrupt decrease in FHR
• An abrupt decrease in FHR is defined as from the onset to FHR nadir < 30 sec
• Decrese in FHR is calculated from onset to nadir
• Decreese in FHR is >/= 15 bpm , lasting > 15 sec and < 2 min in duration
• Onset , depth and duration commonly vary with successive contraction
It is the most common deceleration pattern observed during labour
 Variable deceleration with “shoulders” of acceleration before and after the deceleration
component
-- caused by differing degrees of partial cord occlusion
Occlusion of only vein  decrease fetal blood return  baroreceptor mediated acceleration
Complete cord occlusion  fetal systemic hypertension  baroreceptor mediated
deceleration
Aftercoming shoulder – represents same events occurring in reverse
Mediated vagally
Vagal response may be due to chemoreceptor or baroreceptor activity or both
Partial/complete cord occlusion  increase in after load (baroreceptor )& decrease in fetal
arterial oxygenation (chemo receptor )  vagal activity  deceleration
Recurrent variable deceleration with absent variability are abnormal
 SALTATORY PATTERN
Rapidly recurring couplet of accelerations and decelerations causing relatively large
oscillations of the baseline fetal heart rate
Cord occlusion
 LAMBDA PATTERN
An acceleration followed by a variable deceleration with no acceleration at the end of
deceleration
Seen in early labour
Mild cord compression or stretch
`
 OVERSHOOT
Variable deceleration followed by acceleration
PROLONGED DECELERATION
Visually apparent decrease in FHR below the baseline
Decrease in FHR below the baseline >/= 15 bpm lasting >/= 2 min but less than 10 min in duration
• Cervical examination
• Uterine hyperactivity
• Cord entanglement
• maternal supine hypotension
• Epidural , spinal or paracervical analgesia
• Maternal hypoperfusion /hypoxia
• Placental abruption
• Umbilical cord knots or prolapse
• Maternal seizures
• Application of fetal scalp electrode
• Impending birth
• Maternal Valsalva maneuver
FETAL SCALP BLOOD SAMPLING

 Illuminated endoscope is inserted through the dilated cervix after membrane rupture
 Skin is coated with silicone gel to cause blood to accumulate
 Incision is made through skin to a depth of 2 mm with special blade
 Blood is collected in heparinized glass capillary tube
 pH of blood is measured promptly
pH of fetal scalp blood is lower than umbilical venous blood
pH > 7.25 – labour is observed
pH 7.20-7.25 – pH repeated within 30 min
pH < 7.20 - another scalp blood sample is collected immediately & prompt delivery
Fewer Caesarean deliveries for fetal distress

Fetal scalp blood lactate is also used as adjunct to pH

equivalent in predicting fetal acidemia
SCALP STIMULATION

 HR acceleration in response to pinching of the scalp with Allis clamp – /digital stroke
Vibroacoustic stimulation

 Fetal HR acceleration in response to vibroacoustic stimulation is recommended as a

substitute for scalp blood sampling
 Electronic artificial larynx placed approximately 1 cm away or directly onto maternal
abdomen
 Response to vibroacoustic stimulation is considered normal if a fetal HR acceleration of
at least 15 bpm for at least 15 sec occurs within 15 sec after stimulation and with
prolonged fetal movement
Fetal pulse oximetry

 Unique pad like sensor is inserted through cervix and positioned against the fetal face
where it is held in place by the uterine wall
 Transabdominal fetal pulse oximeter is also there
 Lower limit of normal fetal oxygenation is considered to be 30
 < 30 % for 2 min or longer – increased risk of potential fetal compromise
 < 30 % in the entire interval between two contraction – fetal distresss
FETAL ELECTROCARDIGRAPHY

 As fetal hypoxia worsens there are changes in T wave and ST segments

 Mature fetus exposed to hypoxia develops an elevasted ST segment with a progressive
rise in T wave height
 Increasing T: QRS ratio reflect fetal cardiac ability to adapt to hypoxia and appears
before neurologuivcal damage
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