CARDIOTOCOGRAPHY

Kevin Marcial I. Aralar

1st Year Resident
 External Fetal monitoring
• Non invasive
• Recommended by FIGO
• As long as fetal HR
can be identified

Cardiotocography: Standards for clinical practice. 2019.

Philippine society of maternal fetal medicine
Internal fetal monitoring • Direct monitoring
• Invasive:
 Spiral electrode
attached to fetal
scalp after RBOW
Techniques
• Prior to attachment of doppler, leopolds maneuver to detect fetal
back, where fetal heart beat is best heard
• Distinguish fetal heart rate from vascular souffle, Adequate amount of
gel
• Tocodynamometer, placed on the uterine fundus
• Lateral recumbent, half-sitting, upright positions preferred
 Paper speed
1cm/min

Paper speed
3cm/min

Cardiotocography: Standards for clinical practice. 2019. Philippine society of maternal fetal medicine
Uterine contraction monitoring
• Quantification of uterine activity
Important to quantitate the amount of uterine activity per unit time.
Montevideo units – equal of greater than 200MVU in active labor
NORMAL – 5 contractions or less in 10 min over a 30 min window
TACHYSYSTOLE - >5 contractions in 10 min, in two successive 10 min periods
Non-stress Test
NON STRESS TEST
Most common
cardiotocographic method of
antepartum fetal assessment
initiated once fetal neurologic
Started at
maturity enables acceleration of 26-28 weeks
the fetal heart rate AOG
whenever a viable fetus is at
increased risk of intrauterine
death
Cardiotocography: Standards for clinical practice. 2019. Philippine society of maternal fetal medicine
Non-stress test
• Reactive NST- good predictive perinatal outcome for once week
• Done when there is no contraction
• No exposure to the stress of uterine contraction
Steps for NST
• Empty bladder
• Woman in reclining position or in left lateral recumbent position
• Monitoring for at least 20 minutes
• up to 40 minutes if the initial 20 minutes does not satisy the criteria for
reactive stress test
Indications for non-stress test
• Diabetes
• Hypertensive disordes
• Fetal growth restriction
• Twin pregnancy
• Post-term pregnancy
• Decreased fetal activity
• SLE
Antiphospholipid syndrome
• Sickle cell disease
• Allo immunization
• Oligohydramnios/
Polyhydramnios
• Hx of Fetal demise
• Preterm prelabor rupture of
membranes
• Others ( Non-immune hydrops,
maternal cyanotic disease
hyperthyroidism, vascular
diseases
• Advanced maternal age
INTERPRETATION OF NON
STRESS TEST
• REACTIVE
• REACTIVE NST WITH
DECELERATIONS
• NON REACTIVE
• SPONTANEOUS CONTRACTION
STRESS TEST
Cardiotocography: Standards for clinical practice. 2019. Philippine society of maternal fetal medicine
Reactive NST
• Two or more accelerations lasting for 10-15 seconds, peaking at least
10-15 bpm above baseline in a 20 minute period
• Normal fetal Oxygenation and absence of fetal hypoxemia
Reactive NST with decelerations

• Classified as variable decelerations: brief and

transient episodes of umbilical cord compression
• Perform sonographic evaluation to search for factors
associated with FHR decelerations
• BPS can provide reassurance of fetal well being
• Decelerations may be due to:
• Oligohydramnios
• Nuchal cord
• Intrauterine growth restriction
photo
Non-reactive stress test
• FHR tracing that does not demonstrate at least 2 qualifying
accelerations after 40 minutes
• Sign of interrupted fetal oxygenation -> metabolic acidemia
Management
• Non-reactive NST
• Ancillary testing
• Repeat testing after 30 minutes
• Perform vibroacoustic stimulation fetal scalp stimulation
• Stimulus 1-2 secs repeted up to 3 times for up to 3 secs
• Perform CST
• Perform BPS to evaluate parameters of well being
Basic features of FHR tracing
• Baseline fetal heart rate
• Variability
• Accelerations
• Decelerations
Baseline Fetal Heart Rate

• Baseline must be for minimum of 2

minutes in any 5-10 minute segment
• Normal FHR baseline: 110-160 bpm
Fetal tachycardia
• FIGO: Baseline value above 160 bpm lasting
more than 10 minutes
• Sympathetic nerves and norepinephrine
Causes
• Fetal hypoxia
• Fetal anemia
• Fetal sepsis
• Fetal heart failure
• Fetal tachyarrhythmia
• Maternal fever
• Maternal hyperthyroidism
• Beta-sympathomimetic drugs
• Parasympathomimetic drugs: Atropine, Hydroxyzine HCl (Iterax),
Phenothiazines
Fetal Bradycardia
• FIGO: baseline value less than 110 bpm
lasting more than 10 minutes
• Parasympathetic nervous system
• Vagal nerve (medulla oblangata)
Causes

• Fetal hypopituitarism with brainstem injury

• Maternal hypothermia
• Prolonged hypoglycemia
• Beta blocker therapy
• Second stage of labor
• Maternal heart rate being recorded in a case of
fetal demise.
Fetal Heart Rate Variability
• Fluctuations in the baseline FHR which are irregular in
amplitude and frequency

• Visually quantified as the amplitude of peak-to-trough in

beats per minute
• Absent: amplitude range undetectable
• Minimal: amplitude range detectable but 5 bpm or fewer
• Moderate (Normal): amplitude range 6-25 bpm
• Marked: amplitude range >25 bpm
Moderate Variability
• Normal- A bandwidth amplitude of 5-25 bpm
• Optimal and adequate tissue oxygenation
Normal Varibility
peak to trough= 20 bpm
Minimal
• Reduced FHR variabilty- <5 bpm for >50 minutes in baseline segments
• Poorer prognosis
 Minimal Variability
peak to trough= <5 bpm
Causes
Maternal
• Medication or drugs
• Morphine, Demerol, Nubain, Stadol,
Nembutal, Alcohol, Methadone
Fetal
• Fetal cycle sleeps
• Fetal CNS abnormalities
• Prolonged fetal hypoxia
• Cardiac anomalies
• Persistent fetal tachycardia
excessive/prolonged
parasympathetic vagal stimulation
ABSENT VARIABILITY

results to low apgar scores – most

important sign of fetal compromise
especially when noted with
decelerations
Increased variability
• Saltatory Pattern
• Increased variability
• Bandwidth amplitude >25 bpm lasting for 30 minutes
Sinusoidal Oscillations
1. Sinusoidal Pattern
• Smooth, regular, undulating signal
• Resembles sine wave with amplitude of 5-15 beats with 3-5
cycles per minute
• Lasts more than 20 minutes without any associated
acceleration
• Causes
• Fetal anemia
• Fetal hypoxia
• Cardiac malformations
• Hydrocephlus
• gastroschisis
Increased variability
2. Pseudosinusoidal pattern
• Jagged “saw tooth” appearance
• Seen in
• Amnionitis
• Narcotic analgesics
• Fetal thumb sucking of mouth movements
Accelerations
• In the FHR > 15 bpm above the baseline
• With onset to peak > 30 seconds
• More than 15 seconds but less than 10 minutes
Factors affecting the Acceleration
• Gestational age
• > 32 weeks
• Peak of 15 bpm or more above baseline with 15 seconds duration
• <32 weeks
• Peak of 10 bpm or more above baseline with duration of 10 sec
• Fetal scalp stimulation
• Release of catecholamines
• Medications
• Decreases accelerations (Demerol, MgSO4, Atropine)
PATHOPHYSIOLOGY
• Partial umbilical cord occlusion
• Umbilical vein is first compressed  fetal
hypotension
• Baroreceptors sensitive to even small in
BP
-> vagal stimulation -> in FHR
Cardiotocography: Standards for clinical practice. 2019. Philippine society of maternal fetal medicine
Clinical Significance
• Reassuring -> sign of neurologic responsiveness
• Fetus is not hypoxemic nor acidotic
• NO FHR ACCELERATIONS -> uncertain significance, not highly
predictive of hypoxia
• NO ACCELERATIONS ->Normal tracing by FIGO criteria IF:
• Normal baseline FHR
• Normal variability
• No repetitive decelerations
Decelerations
• Transient episode of slowing the FHR below the baseline level >15
bpm and lasting 25 sec or more
• If rate is below 110 and duration is >10 mins: BRADYCARDIA
DECELERATIONS
• Types of FHR decelerations
• Early
• Late
• Variable
• Prolonged

Cardiotocography: Standards for clinical practice. 2019. Philippine society of maternal fetal medicine
• Quantification criteria
• Amplitude- nadir of the fall from the
baseline
• Duration- number of seconds from the
beginning to the end of the contraction
• Recurrent- occur for >50% of the uterine
contractions in any 20 minute segment of
the tracing
Early Deceleration (Head compression)
• Visually apparent usually symmetrical gradual decrease and return of
the FHR associated with uterine contraction
• Nadir of deceleration occurs at the same time as the peak of
contraction
• Not associated with fetal hypoxia, acedemia or low APGAR score
Late Decelerations
• Apparent decrease in fetal heart rate
• Amplitude of more than 15 bpm below the baseline but rarely more
than 30- 40 beats per minute
• Onset, nadir and recovery of the deceleration occur AFTER the
beginning, peak and ending of contration respectively
• Causes:
• maternal hypotension
• excessive uterine activity
• Placental insufficiency
 Minimal Variability

(+) LATE Decelerations Baseline FHT: 140-145 bpm

Multiple Fetal movement

Uterine contraction: 3-5 mins,

40-50 secs, moderate to strong
Factors affecting the onset of late
deceleration
• Placental Pathology
• Decrease in uterine blood flow
• Supine hypotension from aortocaval compression-> decrease venous return
• Decreased uterine artery pefusion
• Excessive uterine activity/ tachysystole
• 5 or more contractions in 10 minutes, in 2 consecutive 10 minute periods/
averaged over 30 minutes
• Most common cause of fetal hypoxia
• Meternal or fetomaternal hemorrhage
Factors affecting the onset of late
deceleration
• Abruptio placenta
• Disorders of placental insuffiency
• Chronic hypertension and other hypertensive disorders of
pregnancy
• Postmaturity
• Growth restriction
• Diabetes mellitus
• SLE
• Collagen vascular diseases
Variable decelerations
• Visually abrupt decrease in FHR
• Onset, depth and duration vary with successive contractions
• Usually due to umbilical cord compression
• Onset to nadir :<30 sec
• Decrease in FHR > 15 bp, lasting 15 sec and < 2 min in duration
Etiology
• First stage of labor
• Nuchal cord
• Cord prolapse
• Second stage of labor
• Progression with descent of fetal presenting part
• No change in baseline fetal heart rate and variability
Classification (Based in severity and
duration)
• Mild Variable deceleration: <30 sec duration, not below 70-80 bpm
from the baseline
• Moderate variable deceleration: < 80 bpm, regardless of duration
• Severe variable deceleration: >70 per minute with duration of > 60
sec
Prolonged deceleration
• Visually apparent decrease in FHR below the baseline
• 15 bpm or more, lasting 2-15 mins in duration
• Etiology
• Cord compression
• Continuous cord coil
• Progression of severe variable decelerations
• Occult cord prolapse
• Profound uteroplacental insufficiency (Maternal hypotension)
• Paracervical block
• Abruptio placenta
• Maternal hyposia (Seizure, respiratory blockade, MgSO4 toxicity)
Classifications
 NORMAL SUSPICIOUS PATHOLOGICAL
Baseline 110-160 <100 bpm

Lacking of at least one characteristic of

normality, but with no pathological features
Variability 5-25 Reduced variability, increased
variability or sinusoidal pattern

Decelerations No repetitive Repetitive late or prolonged

decelerations decelerations during >30 min
or 20 min if reduced variability
or one prolonged deceleration
with >5 min

Interpretation Fetus with no hypoxia Fetus with a low probability of having Fetus with a high probability of
or acidosis hypoxia/acidosis having hypoxia/ acidosis

Clinical No intervention Action to correct reversible causes if Immediate action to correct

Management necessary identified, close monitoring or additional reversible causes
methods to evaluate fetal oxygenation If not possible expedite delivery

FIGO Cardiotocography Classification

Pathological CTG
• High probability of hypoxia and acidosis-> immediate delivery is indicated
1. Fetal bradycardia (<100 bpm)
2. Reduced Variability (< 5bpm for more than 50 min or more than 3
minutes during decelerations)
3. Increased variability/ saltatory pattern (>25 bpm for more than 30 mins)
4. Sinusoidal pattern (5-15 bpm and frequency of 3-5 cycles per minute)
5. Repetitive decelerations (>50% of contractions)
6. Prolonged deceleration (last > 3 mins)
 ACOG Guidelines
FHR tracing include all FHR tracings include
FHR tracings
Category I

Category III
Category II
the ff: either:
- Baseline FHR 110- include all FHR
- Absent FHR
160bpm tracings not variability and any of
- Baseline FHR categorized as the ff
variability: moderate
CAT I or II -- recurrent late
- No late or variable decelerations
decelerations
- With or without early
--recurrent variable
decelerations decelerations
- With or without -- bradycardia
accelerations - Sinusoidal pattern
Intrauterine Fetal Resucitation
Goal
• Reverse fetal hypoxemia completely or at least improve it adequately
to allow labor to progress
• To buy time in the process of preparing for operative intervention
• To optimize the fetal status at birth during the preparation for surgical
birth
LATERAL POSITIONING
• The most common and easiest to accomplish intrauterine
resuscitation technique in most clinical situations
• Have shown benefit in almost all situations associated with fetal
heart rate changes
• Should be initiated as the first response to a non- reassuring or
abnormal fetal heart rate pattern
• “studies have shown no significant differences in fetal status
between left and right positions”-Simpson et.al, 2005 ‘

• Position change irrespective whether left or right, can

improve fetal heart rate abnormalities produced or
exacerbated by decreased uterine blood flow usually
secondary to supine positioning and inferior vena cava
compression
INTRAVENOUS FLUIDS
Maternal intravascular Fetal oxygen
volume
saturation increased
with at least 500ml
bolus of Lactated
Uterine perfusion
Ringers solution
over 20 minutes in a
normotensive
Fetal oxygenation woman
Cardiotocography: Standards for clinical practice. 201. Philippine society of maternal fetal medicine
Intravenous fluids
• Fetal oxygen saturation was significantly increased after at least a
500 ml bolus of Lactated Ringer’s solution over 20
minutes in normotensive women with increase in fetal
oxygen saturation greatest with 1000 mL IV fluid bolus

• The positive effects on fetal oxygen status continues for more

than 30 minutes after the IV fluid bolus
OXYGEN ADMINISTRATION
Increasing maternally inspired oxygen

Increase in blood oxygen tension

Increase in the delivery of more oxygen to the fetus

When oxygen is given to the mother, there is a more rapid increase in

fetal oxygen saturation as compared to the decrease in fetal oxygen
saturation when it is discontinued.

This indicated the fetus reacts to the new placental oxygen gradient by
accepting oxygen more rapidly
OXYGEN ADMINISTRATION
OXYGEN ADMINISTRATION
FOR FETAL DISTRESS
Not enough evidence to support use if
prophylactic oxygen therapy for women in labor
to prevent nor to evaluate its effectiveness for
fetal distress
 UTERINE CONTRACTION

REDUCTION DECREASE
COMPRESSION of
in the placental maternal-fetal gas
myometrial vessels
blood flow exchange

OXYGENATION resumes 90 seconds after the onset of each contraction

REDUCTION IN UTERINE CAVITY
• Uterine activity produces an intermittent cessation of maternal
intervillous placental blood flow where oxygen exchange occurs
• In normal situations, the remaining oxygen in the villous lakes
and the oxygen supplies of the fetus are sufficient for the fetus to
tolerate this without any change in fetal oxygen saturation
• However, when there is excessive uterine activity, this
intermittent interruption of blood flow reaches a critical level and
the fetus is at risk for hypoxemia
REDUCTION IN UTERINE CAVITY
REDUCTION IN UTERINE
CAVITY
✔To achieve a more rapid reduction in uterine activity,
administration of tocolytics may be used as a temporary
measure to provide intrauterine resuscitation
✔The most commonly used tocolytic is Terbutaline
0.25mg given either subcutaneously or intravenously
AMNIOINFUSION
AMNIOINFUSION
• In patients with a high amniotic fluid volume and variable
heart rate decelerations, the probable cause of the variable
pattern is a nuchal cord so amnioinfusion is less likely to be
helpful
• Furthermore, clinical trials have confirmed that there is NO
physiological reason to expect that it will resolve patterns of
late decelerations, isolated tachycardia or fetal heart rate
patterns with minimal to absent variability
AMNIOINFUSION
CONCLUSION
• CTG is operator dependent
• Routine antenatal cardiotocography is not recommended for
low risk pregnant women to improve maternal and perinatal
outcomes
• The use of routine antenatal and continuous intrapartum
cardiotocography is still dependent on the physician’s sound
clinical judgement whether done to screen for fetal
hypoxemia in a high risk pregnancy or to monitor a fetus with
suspected fetal compromise
CONCLUSION
• PRIMARY GOAL
• Prevent prolonged fetal hypoxemia/ acidemia
• Unnecessary obstetric intervention
• Intrauterine fetal resuscitation allows clinician to
optimize fetal condition
• If the situation does not revert and the pattern
continues to deteriorate, despite the various
resuscitation described, consideration needs to be
given for IMMEDIATE DELIVERY