Transcript CTG

Cardiotocography
CTG
By
Dr. Malak Mohammed Al-Hakeem
Assistant Professor and Consultant
Dept. Obstetric & Gynacology
The CTG only becomes a valuable
method of fetal monitoring and
assessment of fetal well-being if the
professionals involved are able to
interpret the readings correctly.
During labor CTG is a good indicator
of fetal compromise, particularly if
used in conjunction with fetal blood
sampling.
(Murphy et al 1990).
Factors influence the fetal heart are:1. Medical conditions in the mother, e.g. Diabetes
mellitus, Renal disease.
2. Any pregnancy-related diseases, e.g.
pregnancy-induced hypertension, Rhesus
incompatibility.
3. Identified risk factors occurring in pregnancy,
e.g. intrauterine growth retardation Fetal
abnormality, Antepartum haemorrhage.
4. Gestational period.
5. Progress in labor.
6. Drugs e.g.
* Benzodiazepines (nitrazepam, temazepam)
* Tocolytic agents (ritodrine hydrochoride,
salbutamol)
* Analgesics (pethidine).
6. Posture of the mother throughout the CTG –
lying supine causes a decrease in uterine blood
flow, and a decrease in oxygen transfer to the
fetus.
Fetal distress occurs as a result of an
asphyxial insult which gives rise to
intra-uterine hypoxia.
Fetal hypoxia develops when:
1. Insufficient oxygen is transferred from the
mother to the fetus through the placenta.
2. If the transfer of oxygen is adequate, but
the fetus is unable to utilize it due to, e.g.
impaired circulation.
CTG abnormalities should be considered as an alert
factor to the possibility that the fetus is suffering
some degree of hypoxia. However, this is a
subjective diagnosis.
For the diagnosis to be more accurate, interpretation
of the CTG should be combined with fetal blood
sampling.
(Murphy et al 1990)
Interpreting of CTG:1. Fetal heart
A.
Basic patterns
1. Baseline heart rate
2. Variability
B.
Periodic changes
3. Accelerations
4. Declarations
2. Uterine contractions
* Frequency
* Amplitude
* Duration
Normal CTG:1. The baseline heart rate is 120-160 b.p.m.
2. The variability is 5-15 b.p.m.
3. Accelerations may or may not occur in
response to uterine contractions or fetal
movements.
4. No decelerations occur.
Basic Patterns
* Baseline fetal heart rate is regulated by:1. Autonomic nervous system (sympathetic +
parasympathetic.
2. Aortic arch receptors (chemoreceptors +
Baroreceptors).
3. Gestational age.
*
Baseline fetal heart rate is
controlled by:-
1. Autonomic nervous system.
_____________________
Sympathetic
activity results in
bradycardia.
-
Parasympathetic
activity, mainly
the vagus nerve,
results in bradycardia
In normal circumstances, the vagal activity is
dominant, exerting a constant slowing of the
heart rate, stabilizing it at
120-160 b.p.m.
2. The baseline fetal heart is also
controlled by receptors in the
aortic arch:
1. Chemoreceptors, which are stimulated by changes
2.
in oxygen levels. An acute fall in oxygen levels leads to
an increase in parasympathetic activity, resulting in a
slowing of the heart rate. A more prolonged fall will lead
to chronic changes and an increase in sympathetic
activity, resulting in a rise in the heart rate.
Baroreceptors, which are stimulated by changes in
arterial pressure. Hypertension leads to an increase in
parasympathetic activity, resulting in a slowing of the
heart rate. Hypotension leads to an increase in
sympathetic activity, resulting in a rise in the heart rate.
3.
Gestational Age:
The baseline heart rate is related to
gestational age and the maturity of the vagus
nerve. The more mature the fetus, the more
evident the slowing effect that the vagus
nerve exerts upon the heart rate becomes.
Baseline abnormalities:1.
Baseline bradycardia Bradycardia is
defined as a baseline being a
persistently low baseline of below 120
b.p.m.
Causes of Baseline Bradycardia:
Many baseline bradycardias have no identifiable
cause.
1
2
•
•
Gestational age of grater than 40 weeks.
Postmature fetuses have a marked vagal
tone, causing a slowing of the heart rate.
Cord compression. Causes acute hypoxia
leads to bradycardia.
Congenital heart malformations.
Certain drugs, e.g. benzodiazepines.
Baseline abnormalities:2.
Baseline tachycardia
Definition
Baseline tachycardia is defined as being a
persistently high baseline of above 160 b.p.m.
Causes of baseline tachycardia:1. Maternal stress and anxiety will release
catecholamines, stimulating the
sympathetic nervous system, resulting in
an increase in both maternal and fetal
heart rates.
2.
Gestational age. CTG at 32 weeks or below can show a
baseline tachycardia due to the immaturity of the vagus
nerve. The sympathetic nervous system is dominant,
resulting in a persistently high fetal heart rate.
3.
Maternal pyrexia. Leads to maternal tachycardia.
Mothers can develop a pyrexia in labor unrelated to
infection, particularly if the labor has been long, and
signs of maternal distress or obstructed labor are
evident. However, with modern management of labor,
this should rarely, if ever, be seen. When fetal
tachycardia is diagnosed, infection should always be
considered.
4. Fetal infection. During infection, oxygen
requirements are raised. The heart rate rises to
increase the oxygen transfer around the body.
•
Fetal tachycardia is the first sign of
choriomniotritis.
5. Chronic hypoxia. Leads to an increase in the
sympathetic activity, resulting in a rise in the
heart rate. In this instance, the tachycardia may
also be complicated by a decrease in
variability.
6. Fetal hormones.
The fetus, in response to stressful situations,
e.g. a decrease in oxygen levels, produce
epinephrine and norepinephrine from the
adrenal glands. Their effects is similar to
an increase in sympathetic activity, i.e. a
rise in the heart rate. Therefore, a
baseline tachycardia can also be the initial
response to fetal hypoxia.
Variability
Definition
*
Variability is due to interaction between
all the systems (autonomic nervous
system + aortic arch receptors.) It occurs
as a result of the beat-to-beat changes
in the heart rate.
*
Normal variability is between 5-15 b.p.m.
Normal variability represents an
intact nervous pathway through
the cerebral cortex, midbrain,
vagus nerve and cardiac
conduction system.
Variability can be analyzed as being:
1. Normal
2. Increased
3. Decreased
Increased variability
Causes
The initial fetal response to acute
hypoxia may cause a transient increase
in variability due to stimulation of the
parasympathetic nervous system.
Decreased variability
Causes
1. Fetal sleep.
This pattern should not persist for
longer than 30 minutes.
2. Drugs. E.g. Pethidine, sedative
drugs it should not persist for
longer than 30-40 minutes.
3. Gestational age.
At 28-30 weeks decreased variability due to
immaturity of autonomic nervous system.
4. Hypoxia:
Causes reduction in the transmission of
impulses through nervous system, leads to
decreased variability.
Sinusoidal pattern
Sinusoidal patterns are uncommon, occurring
in only 0.3% of monitored, labors.
Definition
This pattern is identifiable by its distinctive
smooth, undulating sine-wave-like baseline.
Beat-to-beat variability is absent.
Aetiology of sinusoidal pattern:1. Idiopathic.
A.Fetal thumb sucking.
B.Narcotic analgesia. It should not persist
more than 20-30 minutes.
2. Anaemia.
A. Rhesus incompatability.
B. Twin-to-twin transfusion.
C. Large feto-matemal bleed.
3. Cord compression.
Resulting in alternating hypervolaemia and
hypovolaemia.
Periodic Changes
Accelerations
Definition
Is an increase in the fetal heart rate of 15 b.p.m. or
more, lasting for at least 15 seconds.
Accelerations occur in a response to either a fetal
movement or a uterine contraction.
When accelerations occur the CTG is said to be
reactive.
Aetiology
Acceleration is caused by the interaction of
the sympathetic and parasympathetic nervous
systems as a result of an increase in
metabolic demands of the fetus during an
active phase, or during a uterine contraction.
Decreased reactivity.
Causes:
1. A period of fetal sleep.
2. Drugs e.g. sedative or analgesia. Methods
of fetal stimulation, e.g. abdominal
palpation or giving the mother cold water
to drink, can evoke a response in the
fetus.
Decelerations
Decelerations of the fetal heart rate from the
baseline can be classified into three types:
1. Early deceleration
2. Late deceleration
3. Variable deceleration
Early decelerations
Definition.
The onset of the deceleration is at the onset
of the contraction.
The heart rate reaches its lowest point at the
peak of the contraction and has recovered to
the baseline by the end of the contraction.
Aetiology:Compression of fetal head during uterine contraction.
(A)
In intracranial pressure
(B)
Pressure on
Cerebral blood flow and
oxygenation
Vagal centre in the brain
02 tension is detected by
cerebral chemoreceptors
Parasympathetic activity
Fall in the fetal heart rate
Late decelerations
Definition.
Any deceleration whose lowest point occurs
more than 15 seconds after the peak of the
contraction is said to be late.
Aetiology.
Late decelerations arise as a result of a
decrease in uterine blood flow and oxygen
transfer during a uterine contraction.
The decelerations occur after the contraction
due to the time it takes for the circulating
blood to reach the aortic arch from the
placenta.
Causes.
1. A reduction in placental blood flow e.g.
(abruption, maternal hypotension,
excessive contractions).
2. Maternal diseases e.g. D.M., HTN, renal
disease.
3. Compromised fetus e.g. IUGR, prematurity, twin to twin transfusion.
Variable decelerations
Definition.
Variable decelerations are inconsistent in
shape and in their relationship to uterine
contractions. Accelerations often precede and
follow the deceleration.
Aetiology.
Transient compression of the umbilical cord,
between the fetus and surrounding maternal
tissues or fetal parts, during a uterine
contraction.
Cord Compression
The effect of variable decelerations upon the
fetus varies depending upon the duration and
degree of cord occlusion that occurs during a
contraction.
Management of deceleration:
Early decelerations:
This is aimed at relieving the
pressure on the fetal head during a
uterine contraction. Changing the
maternal posture is normally all that
is required.
Management of late and variable
decelerations:
The aim is to increase the uterine blood flow and oxygen
transfer across the placenta to the fetus.
1.
2.
3.
4.
5.
6.
7.
Change maternal posture.
Increase or commence intravenous infusion.
Give facial oxygen.
Stop any oxytocic infusion if in progress.
Vaginal examination to exclude cord prolapsed.
A fetal blood sample should be obtained to assess the pH value and
base deficit of the fetal blood.
Whilst the above actions are being undertaken, the mother should
be prepared for delivery.
Thank you