Cardiotocography

CTG

By

Dr. Malak Mohammed Al-HakeemAssistant 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).

7. 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 patterns1. Baseline heart rate

2. Variability

B. Periodic changes3. 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 Parasympathetic activity results in activity, mainly

bradycardia. 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 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.

2. 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 Gestational age of grater than 40 weeks. Postmature fetuses have a marked vagal tone, causing a slowing of the heart rate.

2 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 variabilityCauses

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.

AetiologyAcceleration 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.

DecelerationsDecelerations of the fetal heart rate from the

baseline can be classified into three types:

1. Early deceleration

2. Late deceleration

3. Variable deceleration

Early decelerationsDefinition.

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) (B)

In intracranial pressure Pressure on

Cerebral blood flow and Vagal centre in the brain

oxygenation

02 tension is detected by

cerebral chemoreceptors

Parasympathetic activity

Fall in the fetal heart rate

Late decelerationsDefinition.

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, pre-maturity, 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 CompressionThe 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. Change maternal posture.

2. Increase or commence intravenous infusion.

3. Give facial oxygen.

4. Stop any oxytocic infusion if in progress.

5. Vaginal examination to exclude cord prolapsed.

6. A fetal blood sample should be obtained to assess the pH value and base deficit of the fetal blood.

7. Whilst the above actions are being undertaken, the mother should be prepared for delivery.

Thank you