Cardiotocography

V. Gintautas, G. Ramonienė, D. Simanavičiūtė

 Cardiotocography (CTG) – is defined as the graphic recording of fetal heart rate and uterine contractions by the use of electronic devices indicated for the assessment of fetal condition.

It was found that the use of CTG does not improve perinatal the indicators in the presence of low risk pregnancy/delivery, nevertheless, if pregnancy is considered to be high risk – a precise diagnosis in respect to fetal hypoxia or acidosis can be established by the use of  CTG.
The majority of females, who received a CTG, evaluated this methodology for the assessment of fetal condition. as “favorable”.

Methods of CTG recording

A cardiotocograph (Fig. 1) records the fetal heart rate (cardiotacho) and alterations in the uterine muscle tone curve (tocodynamo) simultaneously. 

    Fig. 1. Cardiotocography
A – curve of fetal heart rate (HR)
B – curve representing alterations in the uterine muscle tone

The fetal HR can be recorded by application of a Doppler Transducer to the maternal abdominal wall at the fetal cardiac projection (Fig. 2).
The use of a doppler transducer during pregnancy or labor is convenient  but some disadvantages should be mentioned: recorded changes in fetal HR are not precise and in some cases (especially when the fetus is dead) the sensor may capture not the fetal HR, but the maternal abdominal aortic pulsation instead.

For those reasons mentioned above, a direct fetal electrocardiography characterized by the application of an electrode into the fetal scalp skin (Fig. 3) may be required during labor. Placement of fetal scalp electrode (FSE) is rarely indicated, unless conventional CTG recording is difficult to perform or  precision of CTG results are suspect. The fetal scalp electrode can only be placed once fetal membranes are ruptured and cervix dilation is at least 2-3 cm.

Alterations in the uterine muscle tone are recorded by a sensitive pressure transducer, which is placed at the uterine fundus. It also records various fetal movements simultaneously. The regular CTG paper speed is 1 cm/min.

Fig. 2. Attachment and fixation of  doppler and pressure transducer to the maternal abdominal wall with belts

Fig. 3. A direct electrode (FSE), which is rotated into the fetal scalp skin

The basic concepts of CTG
Assessment of CTG results is achieved by evaluation of its three main components: basal frequency
(predominating), variability and short-term changes (accelerations and decelerations). It is  necessary to understand the basic concepts of CTG.
Instantaneous frequency – refers to the fetal HR at a given moment, in other words, the fetal HR in every cardiac cycle. The machine measures the duration of each cardiac cycle and converts the results into frequency / minute.
 
Basal frequency (BF)  is  the most common predominating instantaneous frequency on CTG.
It refers to the mean level of fetal HR around which instantaneous frequency alterations take place.
The basal frequency is assessed between “the gaps” of short term changes. The normal BF of a full term fetus ranges from 110 – 150 beats/min. Fetal tachycardia is approved once BF ≥150 b/min.
Fetal bradycardia is approved once BF ≤ 110 b/min.

Variability
The duration of the cardiac cycle is different for each fetus and is constantly changing. These changes are termed instantaneous frequency variability or simply “variability”.
Variability is composed of two components: short-term and long-term variability.
Short-term variability, which is also known as beat-to-beat variability is composed of changes in the fetal HR  between each adjacent cardiac cycle. These changes are minor – ranging from 1 – 5 b/min. Due to these changes, the CTG curve has  rather jagged than straight appearance.
Long-term variability is composed of acceleration or deceleration waves (oscillations), which ranges from several to several tens of cardiac cycles.
One oscillation makes up an entire acceleration and deceleration wave in respect to the BF.
The normal oscillation count ranges from 3-6 b/min with an amplitude of 6-15 b/min and rarely exceeds it.
Both variability components are inextricably linked to each other. They form a coherent cardiac rhythm circuit - cardiotochogram. A numerous  expression of late-term variability oscillation amplitude is as follows: normal variability - 6-15 b/min; decreased - 3-5 b/min.; absent - ≥ 2 b/ min; increased ≥ more 25 b/min.

Due to the presence of short-term variability, only the presence or absence of a sinusoid rhythm can be noted.
The presence of normal variability (Fig. 4) implicates adequate cadiac work regulated by the nervous system, cardiac conducting system and  myocardium, which is not affected by hypoxia.
Despite the existence of other cardiotocographic changes (tachycardia, bradycardia, decelerations), presence of normal variability mitigates the pathological significance of those changes mentioned above and suggests that hypoxia triggers are temporary only, thus the fetus still has reserves for compensation.

Fig. 4. Normal variability

Decline in variability (Fig. 5) during physiological fetal sleep after administration of suppressive drugs.

Fig. 5. Decline in variability

Absence of variability (Fig. 6) is considered to be a poor prognostic sign. It may suggest the presence of fetal nervous, humoral and cardiac autoregulation disorders resulting from persistent hypoxia and acidosis.

Fig. 6. Absence of variability

In some cases variability may increase due to acute hypoxia and umbilical cord compression (Fig. 7).

Fig. 7. Increased variability

The sinusoid rhythm composes a seperate fetal heart rate type (Fig. 8).
It is characterized by the absence of short-term variability, while long-term oscillations are of the same amplitude (5-15 b/min) and same frequency (2-5 b/min), thus similar to the sinusoid rhythm.
A sinusoid rhythm is rarely recorded in case of fetal anemia.

Fig. 8. Sinusoid rhythm

The sinusoidal rhythm should be not confused with a pseudosynusoid rhythm, which is a normal variant of slow variability. In the presence of pseudosynusoid rhythm – oscillations are less monotonous and what is most important, the instantaneous variability shows no absence.

Short-term changes in the CTG (acceleration and deceleration)

Unlike the basal frequency and variability that remain constant for some time the maximal duration of short-term changes is approximately 10 min. Both the acceleration and deceleration time are very different – ranging from several seconds to several minutes with a different amplitude (10 to 30-50 t./min.)
Accelerations are  defined as a short and rapid increase in fetal HR (Fig. 9).
It is the cardiac response to fetal movements, also known as the “Myocardial Reflex”, characterized by an increased HR in response to physical activity.
Accelerations may not only be triggered by fetal movements alone – other methods include: external mechanical or auditory stimulation of the fetus via the maternal abdominal wall. Internal stimulation is possible as well; it refers to the gentle application of pressure on the fetal skin (presenting fetal part) via the vagina. Periodic accelerations are sometimes recorded but rarely during delivery. Those are considered to be a fetal reaction to uterine contractions.

Fig. 9. Accelerations

Decelerations are defined as a short-term decline in fetal HR. Decelerations, which occur after each uterine contraction, are considered to be periodic decelerations.
Given two main factors - deceleration form and relationship between decelerations and the onset and the end of the uterine contraction,  decelerations are classified into three main groups: variable, early and late (Fig. 10).

Fig. 10. Classification of periodic decelerations:
A – early decelerations; B – late decelerations: C – variable decelerations

Early decelerations are uniform and their onset and cessation is equivalent to the beginning and the end of the uterine contraction. This type of decelerations may be due to an increased fetal intracranial pressure (ICP) during uterine contraction. An increased fetal ICP causes mechanical irritation of n. vagus (x) nucleii in the truncus encephali, thus a decline in fetal HR can be observed.
Reflective decelerations, which are n. vagus induced, can not be considered as a symptom of hypoxia.

Late decelerations are uniform, the onset of the deceleration occurs after the beginning of the contraction, and the nadir of the contraction occurs after the peak of the contractions. The fetal heart rate does not return to fetal baseline heart rate and is frequently delayed. A shape of irregular cup with slowly ascending right amplitude is characteristic of these decelerations (nesu tikra)
It is assumed that late decelerations are the result of chronic fetal hypoxia, which is predominantly caused by chronic placental insufficiency. This pathology is characterized by insufficiency of fetal and placental compensatory mechanisms regarding compensation of an additional circulation disorders of the intervillous space during uterine contractions. As a consequence the fetal HR declines.

Late decelerations represent a serious clinical situation, despite their depth. Those are in particular dangerous if recorded after each uterine contraction with a reduced or absent variability.

Variable decelerations
Are polymorphic and their onset is not equal regarding the onset of the uterine contraction.
Those are the most common (> 80%) recorded decelerations during labor characterized by a rapid decline in fetal HR by several tens b/min followed by a faster or slower return to the baseline.
The formation mechanism of variable decelerations goes back to a disorder in fetal hemodynamics, caused by umbilical cord compression.
Initially, the decline in fetal HR is reflectory in origin (irritation of baroreceptors), while later, a decline in fetal HR results from hypoxia. Variable decelerations are classified into typical and atypical decelerations.

Typical variable decelerations are composed of the initial acceleration, a rapid decline in HR to its lowest point followed by a fast return to the basal frequency. A compensatory acceleration is recorded afterwards. Typical variable deceleration is reflectory in origin caused by short-term circulatory disorder in the umbilical cord.

In the course of labor  typical variable decelerations may become deeper and atypical elements may appear including the following: disappereance of primary and compensatory accelerations, HF is slowly returning to its baseline, decelerations are becoming biphasic, disappereance of variability.

Those variable decelerations are known as atypical decelerations. A decline of the fetal HR till 70 b/min and duration of decelerations for ≥ 60 min confirm a suspicion about fetal reserves and well- tolerated labor.

CTG during pregnancy

CTG during pregnancy refers to the performance of the non-stress-test (NST).
The essence of the test is to determine whether an increase in fetal HR (acceleration) is recorded in the presence of fetal movements. A fetus, who is responding by an increase in HR in repsect to his/her own body movements is considered to be “reactive”, thus a non-responding fetus is considered to be non-reactive.

It is desired that the pregnant female is normoglycemic during performance of the NST, as hypoglycemia may have an effect on fetal activity, causing its reduction.
In order to avoid the IVC sindrome, the female is placed on her left side and supine positions are avoided. Transducers are applied to the female’s abdominal wall and fixed with special belts.
The initial recording time is 10 min. The test is discontined if ≥ 2 accelerations of sufficient amplitude (≥ 15x/min) and duration (≥ 15 sec) are found during the first 10 min.
The test is continued for 10 more minutes if no accelerations or only one acceleration was present.

Fetal stimulation may be applied in two ways: by gentle mechanical stimulation in which the maternal abdominal wall is grasped in the projection of the uterus by your hands and set into motion or by auditory stimulation via a special acustic device.

The NST is prolonged for 20 more minutes if fetal movements and accelerations regarding HR are still absent despite adequate stimulation. The NST is ceased and considered to be non-reactive if no accelerations of sufficient duration and amplitude are recorded within 40 minutes. The NST is reactive (Fig. 11) if ≥ 2 accelerations of sufficient amplitude (≥ 15x/min) and duration (≥ 15 sec) are found once the basal frequency is normal and variability is satisfactory (> 5x/min).

A reactive NST in a low-risk or non complicated pregnancy indicates not only fetal condition during the time of performance but also assures that this condition will be maintained for the next 7 days.

Fig. 11. Reactive non-stress-test (NST)

The NST is considered to be non-reactive if no accelerations of sufficient duration and amplitude are recorded within 40 minutes. If second NST, which is performed after 1-2 hours afterwards, provides evidence of non-reactive findings, then chronic fetal hypoxia (perhaps, due to neuroleptics / other agents causing CNS inhibition) is present. The situation is particularly very serious
when a non-reactive NST is accompanied by the absence of any variability (Fig. 12).

Fig. 12. Non-reactive NST

The prognostic value of the NST is highly dependent on the clinical situation.
The performance of the NST 1x/week is insufficient (despite the presence of reactive results) in the following situations: post-term pregnancy (pregnancy lasting > 41); preeclampsia; fetal growth restriction; DM and other severe maternal disorders.
These pregnant females require CTG testing 2-3x/week.
If necessary – CTG is performed daily or even 2 x/day.
Performance of the biophysical profile is required if the NST remains non-reactive one more time and if indicated, a Doppler US investigation of fetal blood flow (cerebral and other vessels) may be done.
As mentioned previously, CTG does not reduce the perinatal mortality and morbidity in a low-risk pregnancy. On the contrary, an incorrect interpretation and frequently occurring false positive NST may result in the formation of an inadequate stressful situation, which eventually ends by too early termination of pregnancy.
Thus CTG recording is delayed in a low-risk pregnancy till the female is term. It is absolutely sufficient to know that the female perceives fetal movements.

CTG during labor

Placental vascularization may be  reduced due to the increased intrauterine pressure during contractions. Additionally, umbilical cord compression may be present as well, thus various alterations in fetal HR can be recorded during labor.
Intrapartum CTG aids in evaluation of labor progress implicating frequency, duration, and relative intensitiy of uterine contractions.

Indications for CTG:

• Alterations in fetal HR present during auscultation;
• High-risk delivery (Table 1);
• Induced or/and stimulated labor;
• Auscultation can not be performed due to maternal body composition or various other reasons.

Table 1. Risk factors representing an indication for CTG use

Interpretation and evaluation of CTG results

There are three main cardiotocographic signs, which are distinguished: permissible, warning and threatening signs. The cardiotocogram is classified as normal, questionable and pathological (Fig. 2, 3).

Table 2. Categories of fetal HR signs

Table 3. Characterization of cardiotocogram

Examples of normal (Fig. 13, 14), questionable (15, 16, 17) and pathologic (18, 19, 20, 21) cardiotocograms are provided.

Fig. 13. Normal cardiotocogram

Fig. 14. Normal cardiotocogram

Fig. 15. Questionable cardiotocogram: Early decelerations

Fig. 16. Questionable cardiotocogram: typical variable decelerations

Fig. 17. Questionable cardiotocogram: tachycardia

Fig. 18. Uterine hyperdynamics as well as atypical variable decelerations

Fig. 19. Pathological cardiotocogram: late decelerations and absence of variability

Fig. 20. Pathological cardiotocogram: absence of variability (table indicates fetal hypoxia)

Fig. 21. Pathological cardiotocogram: sinusoid rhythm and atypical variable decelerations (indicates fetal anemia)

• The female has to change her position – changing her position from one side to the other, may prevent umbilical cord compression as well as IVC syndrome. A supine position during labor should be avoided.
• Administration of O2 8-10 l/min – may be used for short terms only and its efficacy is not proved.
• If CTG changes occur after stimulation of labor – stimulation must be terminated.

Once alterations have disappeared, intravenous Oxytocin can be continued at a slower speed.

• Infusion therapy with physiologic or Ringer solution as placental perfusion improves in the presence of an increased circulating maternal blood volume. Infusion therapy is in particular effective in cases of maternal dehydration.
• If CTG changes occur in the presence of too strong labor activity – tocolytic agents may be administrated for reduction of uterine contractions. Tocolytic agents are proven to improve the fetal state even in the absence of increased labor activity.

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