OG 2.

2
Anatomy of the Female Pelvis

OG 1.8 THE CARDIOTOCOGRAPH

Class Senior Cycle 1
Course Obstetrics and Gynaecology
Code SC1 Obs
Title CTG
Date January 2015
Department of Obstetrics & Gynaecology
Department of Anatomy
Royal College of Surgeons in Ireland
 Background of CTG
Pioneered in 1958 by Hon.in USA and
Hammacher in Europe
Commercially available 1968
Continuous monitoring of Fetal heart in
low risk women -lacks evidence
Needs to be viewed in conjunction with
other assessment e.g. Fetal Blood
Sampling and clinical situation.
Should be used for the right reason and
with appropriate degree of skill

Department of Obstetrics &

Gynaecology, RCSI
 Fetal Monitoring
Continuous intrapartum fetal monitoring
since the 1970s
Low risk mothers Continuous EFM
confers no benefit to the fetus (McDonald et al 1985)
and increases obstetric intervention (NICE 2004,
Mongeli at al 1997, Supplee & Vezeau 1996, Thacker et al 1995)

Most common reason for Caesarean (CS) is

presumed fetal compromise
Indirect link between CS rates and
Maternal Mortality (Hall 2001)
Department of Obstetrics &
Gynaecology, RCSI
Continuous Fetal Monitoring (CFM)

Pros Cons
Can increases CS rate by 1.4%
Can increase instrumental
rate by 1.2%
Reduction in No change in Cerebral palsy
neonatal seizures rates
No difference in Apgar scores
by 0.51% Can be difficult to interpret as
50% of Intrapartum CTGs
have 1 abnormal feature

Therefore CFM therefore best avoided in low risk mothers.

Intermittent auscultation is sufficient for women identified as
low risk

Department of Obstetrics &

Gynaecology, RCSI
 Interpretation of the CTG-Important
Background information
Antenatal CTG vrs Intrapartum CTG
Pre- existing maternal medical conditions PIH
etc....
Antenatal Risk factors Rhesus Status, IUGR,
Fetal anomaly, APH, Location of Placenta etc
Gestational age of the fetus
Overall progress in labour
Drugs administered (or self administered!) to the
mother opiates, benzodiazepines, tocolytics
analgesia, anaesthesia, nicotine, alcohol...

Department of Obstetrics &

Gynaecology, RCSI
 Information recorded on the CTG
Maternal Details, Date and Time of recording
Maternal Pulse
Posture of mum
Speed of the paper ( 1cm/min 3cm/min)
Drugs, vaginal examinations, epidural
administration
Following birth, the midwife should sign and
note date, time and mode of delivery on the CTG
The CTG should be stored securely with the
womans notes.

Department of Obstetrics &

Gynaecology, RCSI
Interpretation of CTG Basic Points

Basic Patterns
Baseline Heart Rate
Variability

Periodic Changes
Accelerations
Decelerations

Department of Obstetrics &

Gynaecology, RCSI
Interpretation of CTG Basic Points

CTGs can be classified as normal,

suspicious or pathological

Department of Obstetrics &

Gynaecology, RCSI
Interpretation of CTG Basic Points

Department of Obstetrics &

Gynaecology, RCSI
Reassuring CTG

Department of Obstetrics &

Gynaecology, RCSI
 Baseline fetal Heart Rate -
PHYSIOLOGY
Controlled by
(i) autonomic nervous system
Sympathetic activity tachycardia
Parasympathetic activity vagus nerve bradycardia
Vagal activity is dominant Constant slowing of heart rate to 110
160

(ii) receptors in the aortic arch

Chemoreceptors Acutely decreasing pO - Increased 2

parasymathetic activity Slowing heart rate

Prolonged hypoxia chronic changes increased sympathetic
activity tachycardia
Baroreceptors Hypertension increased parasympathetic activity
Hypotension increased sympathetic activity

Department of Obstetrics &

Gynaecology, RCSI
 Baseline Bradycardia

Baseline persistently below 110 bpm.

Considerations
Gestational age postmaturity
increased vagal tone (90 110 bpm)
Cord compression
Congenital heart malformations and
heart block
Maternal benzodiazepines
Department of Obstetrics &
Gynaecology, RCSI
 Baseline Tachycardia
Persistently high baseline >160bpm

Considerations
Excessive fetal movements
Maternal stress/ anxiety catecholamines
Gestational age ( fetus < 32 weeks vagal immaturity)
Maternal Pyrexia
Fetal infection Increases oxygen requirements
Chronic hypoxia may also have decreased variability
Fetal hormones Adrenaline and noradrenaline from
fetal adrenals baseline tachy can be the initial
response to fetal hypoxia
Department of Obstetrics &
Gynaecology, RCSI
 Variability

5-15 beats ( not beats per minute!)

Results from healthy interaction of all
the physiological controls
Good variability - intact nervous
pathway through cerebral cortex
midbrainvagus nervecardiac
conduction system
Normal / Increased / Decreased
Department of Obstetrics &
Gynaecology, RCSI
 Decreased Variability

Fetal Sleep (NO LONGER THAN 40 MINS) ,

Fluids, Position
Drugs Pethidine in early labour (NO
LONGER THAN 40 MINS)
Gestational age
SEVERE HYPOXIA autonomic nervous
system fails to respond to stress
Decreased variability with betamethasone
( not seen with dexamethasone) Senat at al BJOG
2005

Department of Obstetrics &

Gynaecology, RCSI
Grades of Variability

Department of Obstetrics &

Gynaecology, RCSI
 Sinusoidal Pattern
Uncommon (0.3% of monitored labours) Young et al
Smooth, undulating, sinewave like pattern.....beat
to beat variability absent
Causes
(i) idiopathic thumbsucking, Narcotic analgesia
(<30 mins)
(ii)Anaemia rhesus isoimmunisation, twin to twin,
large APH
(iii)Severe hypoxia - especially traces with an
amplitude of 20 beats or more or frequency of 1-2
oscillations per minute ~ IMMEDIATE DELIVERY O
Connor et al 1980

Department of Obstetrics &

Gynaecology, RCSI
Sinusoidal Pattern

Department of Obstetrics &

Gynaecology, RCSI
 Accelerations

Increase in the fetal heart rate of 15

bpm or more for at least 15 seconds
Either response to fetal movement
(increased metabolic needs) or
uterine contractions
Reactive ( Different to variability)
Decreased reactivity fetal sleep,
sedation, analgesia
Department of Obstetrics &
Gynaecology, RCSI
Accelerations
Acceleration

 Early Decelerations
Uniform in shape, occur with each contraction, appear
as the mirror image of the contraction, onset of the
deceleration is at the onset of the contraction, lowest
point at the peak of the contraction, has recovered by
end of contraction and amplitude of 40 bpm or less.
Causes:
Compression of fetal head and decrease in cerebral
blood flow
Transient hypoxia, not associated with poor
outcome ( in labour)
Change in maternal posture

Department of Obstetrics &

Gynaecology, RCSI
Early Decelerations

Department of Obstetrics &

Gynaecology, RCSI
 Late Decelerations
Late - Uniform in shape and occur after the contraction (lowest
point occurs 15 secs after the peak of the contraction)
Causes:
Decreased uterine blood flow
Abruption
Maternal hypotension
Excessive uterine activity
Placental insufficiency DM, PIH, Renal Disease
The pre-compomised fetus is at increased risk of developing
late decels IUGR, Prematurity, Rhesus Disease, Twin to Twin
Late Decels always associated with significant fetal hypoxia

Department of Obstetrics &

Gynaecology, RCSI
Late Decelerations

Department of Obstetrics &

Gynaecology, RCSI
 Variable Decelerations
Inconsistent in shape and relationship to uterine contractions
Amplitude of 40 bpm or more
Transient compression of the cord, nuchal cord, cord prolapse

Department of Obstetrics &

Gynaecology, RCSI
 Prolonged Decelerations
Drop in FHR of 30 bpm or more for longer than 2 minutes
Decrease in placental Oxygen transfer
Commonly associated with preceeding variable decels.
Total cord occlusion / prolapse
Maternal hypotension - administration of local
anaesthetic via epidural catheter
Uterine hypertonia
After VE or ARM pressure on fetal head pressure on
vagal centre
Important to consider the entire CTG
Consider results of fetal blood sampling along with CTG

Department of Obstetrics &

Gynaecology, RCSI
Prolonged Decelerations

Department of Obstetrics &

Gynaecology, RCSI