Physiology of fetal heart rate control
Normal human labour is characterized by regular uterine contractions and repeated episodes of transient interruption of fetal oxygenation. The fetal heart rate (FHR) pattern is an indirect marker of fetal cardiac and central nervous system responses to changes in blood pressure and acid-base status that occur during labour. Therefore, the most important role of intrapartum FHR monitoring is to assess the adequacy of fetal oxygenation and presence of fetal metabolic acidaemia during labour, so that timely intervention can be undertaken to reduce the likelihood of neurologic injury or death.
FHR is controlled by both autonomic (sympathetic and parasympathetic nervous systems) and somatic components of the central nervous system:
I. Autonomic control of the FHR:
• Sympathetic nerves are distributed throughout the myocardium of the term fetus. Sympathetic stimulation leads to a “fight or flight’ response via cathecolamines release (adrenaline and noradrenaline). This accelerates the FHR, increases baseline variability and improves myocardial contractility.
NB: During fetal life there is no mechanism of improving tissue oxygenation via respiratory rate increase.
• The parasympathetic innervation of the heart is primarily mediated by the vagus nerve, which influences the sinoatrial and atrioventricular nodes. Parasympathetic stimulation slows down the FHR and exerts a progressively greater influence on the FHR as gestational age advances. Parasympathetic activity is mediated via two types of receptors: baroreceptors and chemoreceptors.
1. Baroreceptors (mechanical receptors)
The most important arterial baroreceptors are located in the carotid sinus (at the bifurcation of the internal and external carotids) and in the aortic arch. Changes in fetal blood pressure (for example, umbilical cord compression during uterine contractions) lead to increased peripheral resistance and hypertension that ‘stretches’ the baroreceptors. Once stimulated, the baroreceptors send impulses that lead to a parasympathetic response on the heart rate and a resultant bradycardia.
NB: The baroreceptors mediated decelerations are noted on the CTG as ‘early’ and ‘variable decelerations’ (i.e. head and umbilical cord compression mechanisms respectively). They are short-lasting and the FHR quickly returns to baseline. Their presence is benign, in the absence of other CTG abnormalities. As a result, no other intervention is required except for continuous FHR monitoring.
2. Chemoreceptors
These are found in the aortic and carotid bodies (peripheral) and in the brain (central) and respond to hypoxia, excess carbon dioxide and acidosis. The activation of these receptors also induces a parasympathetic response on the FHR. However, the stimulation of these receptors is prolonged, due to the increased time required to washout the deoxygenated blood from fetal circulation in order to remove the stimulus.
NB: The chemoreceptors mediated decelerations are noted on the CTG as ‘late decelerations’ and have delayed onset with gradual fall form the baseline rate and slow recovery. They are usually associated with fetal metabolic acidosis.
II. Somatic nervous system control of the FHR
FHR accelerations are frequently associated with fetal movement, possibly as a result of stimulation of peripheral proprioceptors, increased catecholamine release and autonomic stimulation of the heart. However, some studies have shown the presence of accelerations even after induction of fetal paralysis and this reflects the integrity of somatic nervous system. [1]
Physiologic significance of selected FHR characteristics
CTG analysis starts with the evaluation of the clinical situation and presence of risk factors, assessment of basic CTG features (baseline, variability, accelerations and decelerations, contractions) followed by overall CTG classification using various international guidelines (FIGO, NICE, ACOG, etc.).
1. Baseline FHR
This is the mean level of the most horizontal and less oscillatory FHR
segments. It is estimated in time periods of 10 minutes and expressed in
beats per minute (bpm). [2] This refers to resting FHR, therefore accelerations and decelerations should be excluded when establishing the baseline FHR.
NB: There are situations where FHR is difficult to establish over a 10-minute time period, in particular during active second stage of labour or during episodes of fetal active wakefulness. In these situations, it is very important to review previous CTG records and/or assess the FHR baseline over a slightly longer period of time.
Normal baseline rate: 110 – 160 bpm
Preterm fetuses tend to have values towards the upper end of this range, whilst term/post-term fetuses towards the lower end (due to the maturation of the parasympathetic system that occurs as the gestational age advances).
Fetal tachycardia: >160 bpm for > 10 minutes [2]
Causes:
o Maternal sepsis (the most common cause) – due to chorioamnionitis or extrauterine infection
o Epidural analgesia – due to transient maternal pyrexia
o Rebound – transient fetal tachycardia following a prolonged deceleration, usually accompanied by reduced variability
o Evolving non-acute fetal hypoxia – initial fetal compensatory mechanism to hypoxia is to increase cathecolamine production by the adrenal glands
NB: When looking at baseline FHR it is very important to assess the trend over time, for example although a baseline FHR of 150 bpm is still within normal range, if this has increased from an initial baseline of 110 bpm at the very start of labour this represents an abnormal feature and the underlying causes should be identified – such as ongoing chorioamnionitis, evolving fetal hypoxia especially if associated with preceding decelerations, etc.
o Drugs – beta agonists (terbutaline, salbutamol, etc.), parasympathetic blockers (atropine, etc.)
o Fetal cardiac causes: tachyarrhythmia – usually > 200 bpm, heart failure (rare)
Fetal bradycardia: <110 bpm for > 10 minutes [2]
Causes:
o Post-term fetuses (usually FHR between 100 – 110 bpm)
o Fetal cardiac causes: heart block
o Drugs – beta blockers
o Maternal hypothermia
o Terminal fetal bradycardia in acute hypoxic events (umbilical cord prolapse, uterine rupture, placental abruption)
2. Variability
This refers to the oscillations in the FHR signal, evaluated as the average bandwidth amplitude of the signal in 1-minute segments [2] and reflects the continuous interaction between sympathetic and parasympathetic systems.
Normal variability: 5-25 bpm
When normal FHR variability is noted, fetal hypoxia becomes unlikely as this implies that both components of the autonomic system are functioning well.
Reduced variability: < 5bpm
Causes:
o Fetal hypoxia/acidosis: especially if preceding or concomitant decelerations and rise in FHR baseline
o Fetal deep quiet sleep phase: usually preceded by normal CTG and not lasting more that 50 minutes with seldom variability < 5bpm
o Drugs: CNS depressants, parasympathetic blockers
o Infection
o Previous fetal cerebral insult (haemorrhage)
NB: There is a high degree of subjectivity in the visual evaluation of this parameter, and therefore careful re-evaluation and second opinion is recommended in borderline situations.
Increased variability: > 25bpm for > 30 minutes [2]
The pathophysiology of this ‘saltatory pattern’ is not completely understood, however it may be seen associated with recurrent decelerations (such as active second stage of labour) when fetal hypoxia evolves very rapidly. A potential underlying mechanism could be fetal autonomic instability and hyperactivity. [3]
3. Accelerations
Accelerations represent abrupt (onset to peak in less than 30 seconds) increases in FHR above the baseline, of more than 15 bpm in amplitude, and lasting more than 15 seconds but less than 10 minutes. [2]
Accelerations coincide with fetal movements and their presence reliably predicts the absence of fetal hypoxia as this reflects the integrity of somatic nervous system. Accelerations elicited by fetal scalp stimulation during vaginal examination have the same ability to exclude on-going hypoxic injury as spontaneous accelerations. [4] When accelerations are induced in this setting, the fetal pH is >7.20 in over 90% of cases, and when no accelerations occur pH is <7.20 in approximately 50% of cases. [8-11]
The absence of accelerations in an otherwise normal intrapartum CTG is of uncertain significance. However, the disappearance of accelerations following the onset of decelerations is a feature of gradually evolving hypoxia. [1]
Before 32 weeks of gestation, the amplitude and frequency of accelerations may be lower (10 bpm amplitude lasting more than 10 seconds) given the physiological immaturity of the fetal heart at this stage. [5]
NB: Accelerations that coincide with uterine contractions, especially when recorded during the active second stage of labour, suggest erroneous recording of the maternal heart rate therefore assessment using fetal scalp electrode is recommended (although still susceptible to artefact). [6]
4. Decelerations
Decelerations refer to a decrease in the FHR below the baseline of more than 15 bpm in amplitude which is lasting more than 15 seconds. [2]
Early decelerations coincide with contractions and are associated with fetal head compression. These decelerations are rare, usually shallow and short lasting with maintained variability during the deceleration. Their presence does not indicate fetal hypoxia.
Variable decelerations are associated with umbilical cord compression and these are the most common type of decelerations. They are V-shaped with rapid drop, maintained variability during deceleration and rapid return to baseline (duration of < 60 seconds). They vary in shape, form and relation to uterine contraction.
Concerning characteristics of variable decelerations include: duration more than 60 seconds; reduced baseline variability within the deceleration; failure to return to baseline; biphasic (W) shape; no shouldering. [7] When concerning features are present, especially if associated with rising baseline and loss of variability, then it indicates that fetal hypoxia is evolving and the ability to compensate for the stress of labour is lost.
Late decelerations occur as a result of utero-placental insufficiency ant they are U-shaped with/without reduced variability within the deceleration. They have gradual onset (>30 seconds) and/or return to baseline.
When contractions are adequately monitored, late decelerations start more than 20 seconds after the onset of a contraction, have a nadir after the acme and a return to baseline after the end of the contraction. [2] These decelerations indicate fetal hypoxia.
5. Contractions
These are bell-shaped gradual increases in the uterine activity signal, followed by roughly symmetric decreases with 45-120 seconds duration. [2]
During contractions there is decreased placental perfusion and as a result a temporary reduction in the feto-maternal gas exchange occurs. The characteristics of the uterine contractions (frequency, intensity, duration) are the key factors that impact on severity of these disturbances. The most important element is the interval between contractions because this when the fetal oxygenation occurs. There is published data to suggest that in spontaneous labour it takes up to 90 seconds after a contraction for fetal oxygenation to be restored, whilst in the oxytocin-augmented labour this recovery period increased to an average of 138 seconds. [12,13, 2]
Hypertonus: contractions lasting more than 60 seconds. [7]
Tachysystole: more than 5 contractions in 10 minutes in two successive 10-minute periods or averaged over a 30-minute period. [2]
Whether spontaneous or iatrogenic in nature, excessive uterine activity can usually be reversed by reducing or stopping oxytocin infusion and/or starting acute tocolysis.
NB: On the CTG only the frequency of the contractions can be reliably appreciated!
Classification and clinical management of FHR patterns: examples of recommendations of selected international organizations
CTG analysis is subject to intra- and inter-observer variability and disagreement, even when well recognized and standardized guidelines are used. The main features that are prone to disagreement are the identification and classification of decelerations, variability assessment and overall interpretation of the CTG as suspicious and pathological. [14, 15, 2]
There are various studies that looked at the correlation between various CTG criteria and hypoxia and acidosis. It is well recognized that when the CTG exhibits normal features, cases of fetal hypoxia or metabolic acidosis have not been documented. On the other hand, when suspicious or pathological CTGs are noted, although they are sensitive indicators of fetal hypoxia they have low specificity and poor positive predictive value. [2]
• FIGO consensus guidelines on intrapartum monitoring (2015) [2]
Normal
Suspicious
Pathological
Baseline (bpm)
110 – 160
Lacking at least one characteristic of normality, but with no pathologic features
<100
Variability (bpm)
5 – 25
Reduced, increased or sinusoidal pattern
Decelerations
No repetitive*
decelerations
Repetitive late or prolonged decelerations (> 3 minutes) for > 30 minutes OR for > 20 minutes if reduced variability
Single prolonged deceleration > 5 minutes
Interpretation
Fetus with no
hypoxia/acidosis
Low probability of hypoxia/acidosis
High probability of hypoxia/acidosis
Clinical management
No intervention necessary to improve fetal oxygenation status
Action to correct reversible causes if identified, close monitoring or additional methods to evaluate fetal oxygenation
Immediate action to correct reversible causes, additional methods to evaluate fetal oxygenation or if this is not possible expedite delivery.**
* Decelerations are repetitive in nature when they are associated with > 50% of uterine contractions.
** In acute situations (cord prolapse, uterine rupture, placental abruption) immediate delivery should be accomplished.
• NICE Intrapartum care for healthy women and babies (2017) –
endorsed by RCOG [7]
CTG features
Baseline (bpm)
Baseline variability (bpm)
Decelerations
Reassuring
110 -160
5 – 25
None or early
Variable decelerations with no concerning characteristics* for < 90 minutes
Non- reassuring
100 -109**
OR
161-180
< 5 for
30 – 50 minutes
OR
> 25 for 15 – 25 minutes
Variable decelerations with no concerning characteristics* for 90 minutes
OR
Variable decelerations with any concerning characteristics* in up to 50% of contractions for > 30 minutes
OR
Variable decelerations with any concerning characteristics* in over 50% of contractions for < 30 minutes
OR
Late decelerations in over 50% of contractions for < 30 minutes, with no maternal or fetal clinical risk factors such as vaginal bleeding or significant meconium
Abnormal
< 100
OR
> 180
< 5 for
> 50 minutes
OR
> 25 for
> 25 minutes
OR
Sinusoidal
Variable decelerations with any concerning characteristics* in over 50% of contractions for 30 minutes (or less if any maternal or fetal clinical risk factors [see above])
OR
Late decelerations for 30 minutes (or less if any maternal or fetal clinical risk factors)
OR
Acute bradycardia, or a single prolonged deceleration lasting > 3 minutes
Category
Definition
Management
Normal
All features are reassuring
Continue CTG (unless it was started because of concerns arising from intermittent auscultation and there are no ongoing risk factors)
Suspicious
1 non-reassuring feature
AND 2 reassuring features
Correct any underlying causes, such as hypotension or uterine hyperstimulation
Perform a full set of maternal observations
Start 1 or more conservative measures*
Inform an obstetrician or a senior midwife
Document a plan for reviewing the whole clinical picture and the CTG findings
Talk to the woman and her birth companion(s) about what is happening and take her preferences into account
Pathological
1 abnormal feature OR
2 non-reassuring features
Obtain a review by an obstetrician and a senior midwife
Exclude acute events (for example, cord prolapse, suspected placental abruption or suspected uterine rupture)
Correct any underlying causes, such as hypotension or uterine hyperstimulation
Start 1 or more conservative measures***
Talk to the woman and her birth companion(s) about what is happening and take her preferences into account
If the CTG trace is still pathological after implementing conservative measures:
obtain a further review by an obstetrician and a senior midwife,
offer digital fetal scalp stimulation and document the outcome.
If the CTG trace is still pathological after fetal scalp stimulation: consider fetal blood sampling/consider expediting the birth take the woman's preferences into account
* Regard the following as concerning characteristics of variable decelerations: lasting more than 60 seconds; reduced baseline variability within the deceleration; failure to return to baseline; biphasic (W) shape; no shouldering.
** Although a baseline FHR between 100 and 109 beats/minute is a non-reassuring feature, continue usual care if there is normal baseline variability and no variable or late decelerations.
*** Conservative measures: encourage the woman to mobilise or adopt an alternative position (and to avoid being supine); offer intravenous fluids if the woman is hypotensive; reduce contraction frequency by reducing or stopping oxytocin if it is being used and/or offering a tocolytic drug (a suggested regimen is subcutaneous terbutaline 0.25 mg).
• NICHD Workshop report on electronic fetal monitoring (2008) –
endorsed by ACOG [4]
Category I
All of the following criteria must be present. Tracings meeting these criteria are predictive of normal fetal acid-base balance at the time of observation.
– Baseline rate: 110 – 160 bpm
– Moderate baseline FHR variability
– No late or variable decelerations
– Early decelerations, accelerations: present or absent
Category III
These CTG tracings are predictive of abnormal fetal acid-base status at the time of observation. Prompt evaluation is indicated and most parturients will require expeditious intervention, such as provision of supplemental oxygen, change in position, treatment of hypotension, and discontinuation of any uterotonic drugs being administered. Category III tracings include either (1) OR (2) below.
(1) Absent baseline FHR variability AND any of the following
– Recurrent late decelerations
– Recurrent variable decelerations
– Bradycardia
(2) Sinusoidal pattern
Category II
FHR tracing does not meet criteria for category I or III and is considered indeterminate. Category II tracings require evaluation, continued surveillance, initiation of appropriate corrective measures when indicated, and reevaluation.
• Physiological CTG – Intrapartum fetal monitoring guideline (2018) [16]
E. Chandraharan et all produced the first guideline that relies on physiology-based interpretation for the assessment of feta wellbeing and not on pattern-recognition.
The authors recommend a step-wise interpretation of the CTG:
– Step 1: The clinical setting (gestational age, antenatal complications, previous CTG traces)
– Step 2: Current clinical situation and indication for CTG
– Step 3: Limits acceptable as normal for the current trace
– Step 4: CTG trace assessment (intrapartum risks, contractions, baseline FHR, variability and cycling, accelerations and decelerations)
– Step 5: Overall assessment of presence of hypoxia and management plan (see table below)
Types of intrapartum hypoxia
All human cells have aerobic metabolism which requires oxygen and glucose in order to produce energy. During fetal life oxygen supply is dependent on maternal respiration and circulation, placental perfusion and exchange across the placenta, fetal circulation. Recommendations from the United Kingdom and the United States include routine cord blood acid base analysis in all deliveries (caesarean/operative vaginal) performed because of fetal compromise or where fetal metabolic abnormality is suspected.
1. Acute
Prolonged decelerations (>3 minutes) cause rapid onset fetal hypoxia and metabolic acidosis. The pH decreases at a rate of > 0.01/minute.
Prolonged decelerations can result from acute interruption of fetal oxygenation at various levels:
– maternal lungs (e.g. maternal hypoxemia in amniotic fluid embolism)
– maternal heart (e.g. acute reduction in cardiac output)
– maternal vascular system (e.g. maternal hypotension)
– uterus (e.g. excessive contractions or uterine rupture)
– placenta (e.g. placental abruption)
– umbilical cord (e.g. cord prolapse).
Immediate clinical assessment is warranted to exclude acute clinical and obstetrical emergencies and institute management plan that may include emergency delivery of the baby.
The majority of prolonged decelerations where the a-priori CTG is normal, there is no acute intrapartum event (see above) and variability within deceleration is maintained recover within the first 6 minutes (up to 90%) and 9 minutes (up to 95%). [1]
NICE [7] recommends to expedite the birth if fetal bradycardia persists more than 9 minutes.
2. Subacute
If the interval between uterine contractions (when fetal oxygenation occurs) is shorter than the duration of the decelerations (when fetal oxygenation is interrupted) then metabolic acidosis develops, with an expected pH decrease at a rate of 0.01/2-3 minutes.
Prompt clinical interventions to correct uterine hyperstimulation, interrupt maternal active pushing if possible or at least diminish it to active pushing with every other uterine contraction can allow time for ‘in-utero’ fetal resuscitation and decrease the need for obstetric operative intervention.
3. Gradually evolving
When a fetus is exposed to a gradually evolving hypoxic stress there it has enough time to develop compensatory mechanisms. The fetus will preserve its energy to maintain oxygenation of the central organs (brain, heart, adrenal glands) and spare movements. Therefore, the first CTG change noticeable on the CTG is loss of accelerations. If the hypoxic stress progresses further, the cathecolamines release cause an increase in the fetal heart rate, in an attempt to improve oxygenation. The peripheral vasoconstriction leads to blood redistribution preferentially to ‘essential’ organs.
When compensatory mechanisms are lost, CTG signs of evolving fetal hypoxia occurs, such as loss of FHR variability, late decelerations, unstable baseline and progressive decrease of the FHR. [1]
4. Chronic
Utero-placental insufficiency (such as pre-eclampsia) can result in chronic hypoxia. As a result, the antenatal CTG can show fetal tachycardia and/or late shallow decelerations with decreased variability.
NB: These fetuses have reduced physiological reserve to compensate for the stress of regular uterine contractions, therefore rapidly evolving decompensation occurs with the onset of labour!