21 Management of Prolonged Decelerations and Bradycardia. Handbook CTG

 21

Management of Prolonged

Decelerations and Bradycardia

◈

Rosemary Townsend and Edwin Chandraharan

Handbook of CTG Interpretation: From Patterns to Physiology, ed. Edwin Chandraharan.

Published by Cambridge University Press. © Cambridge University Press 2017.

Key Facts

A prolonged deceleration indicates a need for urgent assessment and intervention

to improve fetal oxygenation.

Acute hypoxia caused by cord prolapse, placental abruption or uterine rupture

mandates delivery without any delay.

Most prolonged decelerations with an identifiable reversible cause will respond

to conservative measures and recover within 9 minutes and do not require

immediate delivery.

Acute tocolysis is a useful treatment for prolonged deceleration secondary to

uterine hyperstimulation.

In the absence of an irreversible cause (placental abruption, umbilical cord

prolapse and uterine rupture), the most important features of the CTG trace that

predict the likelihood of recovery of an ongoing prolonged deceleration are

baseline variability prior to the onset of deceleration and variability in the first 3Management of Prolonged Decelerations

minutes of deceleration. In addition, if the fetal heart rate (FHR) is maintained

>100 bpm during a prolonged deceleration, the likelihood of acidosis is low.

Conversely, an acute drop in FHR <80 bpm may indicate acute intrapartum

hypoxic insult and may lead to a rapid development of fetal acidosis if this

persists for >3 minutes.

A prolonged deceleration may be secondary to fetal hypoxia caused by reduced

utero-placental perfusion or sustained cord compression. Nonhypoxic prolonged

decelerations may also be seen during profound vagal stimulation, as is seen

with increased intracranial pressure caused by head compression immediately

before delivery of the head,1 and not all prolonged decelerations are associated

with the same degree of neonatal acidaemia.

The outcome for the fetus will depend on the cause of deceleration, the fetal

condition before deceleration and the preexisting placental reserves, and

therefore, it is important to keep the whole clinical picture in mind.

The fetal response to acute hypoxia is a chemoreflex response leading to

prolonged deceleration and increased peripheral resistance.2 The physiological

aim is to reduce oxygenation of peripheral tissues to preserve cerebral and

myocardial oxygenation (intense peripheral vasoconstriction) as well as to

reduce myocardial workload (prolonged deceleration). Although these

mechanisms exist to protect the central organs from hypoxic injury during an

acute hypoxic or hypotensive insult, prolongation of deceleration may result in

cardiac and neurological damage due to a reduction of perfusion pressure.

Anaerobic metabolism takes place in vasoconstricted peripheral tissues with

progressive lactic acid build-up and metabolic acidosis. In addition, carbon

dioxide cannot be eliminated through the placenta during periods of reduced

placental blood flow, causing a respiratory acidaemia. The respiratorycomponent of acidaemia is rapidly eliminated when placental blood flow is

restored, while metabolic acidosis takes longer to correct.

Whereas, in the presence of subacute hypoxia, fetal pH levels fall at a rate of

0.01 per 2–3 minutes, during a period of acute hypoxia, fetal pH drops at a rate

of 0.01 per minute. Increasing levels of fetal acidaemia will eventually lead to a

disruption of cellular enzymes, tissue injury and death.

With a significant reduction in heart rate, there must be a fall in cardiac output,

whatever the cause, since the fetus does not have the capacity to increase stroke

volume to compensate.3 Peripheral vasoconstriction is an early response that

enables the fetus to maintain near-normal levels of cerebral and myocardial

blood flow in the early stages, but if the insult persists, these mechanisms will

fail.

The fetus prioritizes myocardial flow over cerebral blood flow, so the next CTG

change to be observed will be reduced or absent variability as the fetal

autonomic nervous system is compromised. As blood flow to the myocardium

then fails, myocardial function will depend on glycogenolysis, and once the

glycogen stores are depleted, the myocardium will also begin to fail.

This period of time that will result in central organ decompensation will clearly

be shorter in a growth-restricted fetus with lower glycogen stores.

The presence of acute prolonged fall in heart rate requires rapid intervention

from the care team. This does not mean that the response to every prolonged

deceleration should be immediate delivery, and indeed the majority of prolonged

decelerations will respond completely to simple conservative measures before

either the brain or the myocardium is compromised.

Having a well-practiced protocol for the management of prolonged

decelerations will help avoid unnecessary interventions and distress for the

patient while enabling the team to identify quickly those fetuses that will not

respond to conservative measures.Causes of Prolonged Decelerations

The first priority in the management of a prolonged deceleration is to establish the

underlying cause as quickly as possible to facilitate appropriate management. To this

end, it is useful to classify the causes as reversible and nonreversible (see Table 21.1).

Table 21.1 Causes of prolonged decelerations

Reversible Nonreversible

Hypotension Placental abruption

Excessive uterine activity Cord prolapse

Sustained umbilical cord compression Uterine rupture

Nonreversible Causes of Prolonged

Decelerations

There are three important nonreversible causes of acute hypoxia (prolonged

decelerations) that require immediate delivery. Once a nonreversible cause is

identified, it is not appropriate to delay even 2 or 3 minutes to await recovery of

the CTG, and delivery must be accomplished by the safest and most expeditious

route.

These three nonreversible events are cord prolapse, placental abruption and

uterine rupture. In these situations, the compromise to fetal oxygenation is

profound and cannot be reversed by any conservative measures (except in

umbilical cord prolapse where acute tocolysis may relieve the compression of

umbilical cord during uterine contractions). The immediate examination of the

patient to identify these causes should occur simultaneously with intrauterine

resuscitation measures (left lateral position, fluids, stopping oxytocin).

Any assessment of the mother should start with the ABC (airway, breathing,

circulation) approach and include action to correct any abnormality in maternal

oxygenation or cardiovascular stability. Any condition that causes compromiseReversible Causes of Prolonged Decelerations

Maternal Hypotension

Management of Hypotension

to maternal oxygenation may also cause acute hypoxia in the fetus; however, the

management of these conditions is out of the scope of this chapter. Maternal

resuscitation takes priority and, in the context of a primarily maternal condition,

should be all that is necessary to restore fetal oxygenation.

Abdominal examination should take particular note of the tone of uterus, descent

of fetal head or presence of fetal parts. A vaginal examination is necessary to

rule out cord prolapse, to assess vaginal bleeding, receding presenting part and

cervical dilatation should an emergency delivery be indicated.

If any nonreversible cause of acute hypoxia is identified, delivery should be

immediate, and this would usually be by caesarean section. Although, according

to the NICE classification of urgency, a category 1 caesarean section should

accomplish delivery <30 minutes in the setting of acute hypoxia with an

irreversible cause, delivery after 15 minutes is associated with worsening fetal

acidaemia and greater likelihood of admission to the neonatal unit.

Hypotension may occur in labour due to vagal stimulation, dehydration or

peripheral vasodilatation associated with the administration of regional

anaesthesia or a combination of all of these. In the assessment of a patient in the

context of a prolonged deceleration, it is imperative to assess the blood pressure

immediately and institute measures to correct hypotension.

The supine position should be avoided for labouring women because of the

association with aortocaval compression and associated reduced venous return

and myocardial and placental perfusion.

Place the mother in left lateral position.Excessive Uterine Activity (Tachysystole)

Fluid resuscitation (in the setting of dehydration or acute hypotension after

regional anaesthesia administration).

Tachysystole is defined as excessive frequency of contractions with more than

five contractions in 10 minutes for at least 20 minutes or averaged over 30

minutes. This will not always cause fetal hypoxia, and indeed many well-grown

fetuses with adequate placental reserves will tolerate prolonged periods of

tachysystole.

Uterine hyperstimulation is the presence of CTG changes associated with

tachysystole. In the event of CTG changes associated with prolonged hypertonic

contractions or tachysystole, particularly during oxytocin administration, action

should be taken to reduce the frequency and strength of uterine contractions.

The first action should be to stop administration of any exogenous oxytocin (or

removal of prostaglandins). In the presence of minor CTG changes – for example

a rise in baseline or progressively longer decelerations with evidence of

chemoreceptor activation – this may be sufficient.

In severe acute or subacute hypoxia (including prolonged decelerations), acute

tocolysis is often of benefit in rapidly restoring placental perfusion and

reversing fetal hypoxia. Because tocolytics must be administered rapidly in the

setting of a prolonged deceleration, it is recommended that the medication be

stored in an easy-to-access area together with all the necessary equipment for

administration. In our unit, a clearly marked emergency pack containing 250 μg

terbutaline, a needle, syringe and cotton wool is centrally available and has been

useful in reducing time to administration.

Agents suitable for acute tocolysis include β-sympathomimetics such as

terbutaline and ritodrine.4 Because these drugs have been associated with

maternal cardiac side effects when used for tocolysis for preterm labour, some

alternatives have been trialled. There is some evidence that atosiban, a

competitive oxytocin receptor antagonist that is commonly used in the treatmentManagement of Uterine Hyperstimulation

CTG Parameters That Predict Recovery of

Prolonged Decelerations

of preterm labour, may also be of benefit in acute tocolysis.56 There is little

evidence that magnesium sulphate has a role in acute tocolysis. Nitroglycerine

may also be used, but is less effective than terbutaline and is more likely to

provoke maternal hypotension.7

There may be concern regarding the use of tocolytics immediately before

delivery because the uterine relaxant effect could theoretically increase the risk

of postpartum haemorrhage. While there is little evidence on the blood loss in

deliveries where acute tocolysis has been used in labour for fetal compromise,

in the case of tocolysis with terbutaline used to prolong pregnancies affected by

placenta praevia, no significant difference in blood loss has been demonstrated.8

In our clinical experience, no additional measures beyond routine oxytocics are

required after delivery. If there is no response to oxytocics, 1 mg of propranolol

may be administered to reverse the uterine relaxant effect of terbutaline.

After the administration of an acute tocolytic, signs of improvement in the CTG

may be anticipated within 2–5 minutes. This may simply be a return of normal

variability and need not be a complete return to baseline. In certain

circumstances, a second dose may be appropriate. The team should remain on

standby to perform an emergency delivery until it is clear that the CTG has

normalized.

Intrauterine resuscitation

Stop oxytocin administration

Acute tocolysis (e.g. with 250 μg subcutaneous terbutaline)Assessment of CTG Parameters

In a prolonged deceleration with a previously normal CTG and normal variability in the

first 3 minutes of deceleration, recovery can safely be anticipated. In the presence of a

The majority of prolonged decelerations with a reversible cause will respond to

conservative measures before delivery is indicated, and so the approach to the

patient should be reassuring. The CTG features prior to and during deceleration

are related to the chance of recovery, and familiarity with these features can help

identify which patients really need to be transferred to the operating theatre and

which can safely be managed in the delivery room.

The preceding normal variability on the CTG trace is of importance because it

may give information regarding the oxygenation of the fetus prior to the onset of

current insult. In the case of a normal CTG with a stable baseline and normal

variability, the risk of fetal hypoxia is low; therefore, it can be assumed that the

fetus is starting from a normal acid–base balance. Conversely, if the preceding

CTG showed evidence of fetal hypoxia with a rising baseline and reducing

variability, it indicates that the fetus will not tolerate a long period of acute

hypoxia.

The variability on the CTG corresponds to the integrity of fetal autonomic

nervous system, and in most cases variability is preserved in the first minutes of

prolonged deceleration because cerebral oxygenation is maintained by the

redistribution of cardiac output. If there is normal variability in the 3 minutes

before deceleration and in the first 3 minutes of deceleration, then it is highly

likely that the FHR will recover – 90 per cent in 6 minutes and 95 per cent in 9

minutes.

Conversely, if there is reduced variability before prolonged deceleration, then

even after recovery, as many as 44 per cent of fetuses may be compromised, and

consideration should be given to delivery after consideration of the wider

clinical picture.preceding abnormal CTG, particularly with reduced variability, preparations for

emergency delivery should be made.

When Should Delivery Occur?

In the absence of nonreversible causes and after the institution of conservative

measures for intrauterine resuscitation, the key clinical decision to be made is

whether or not to initiate delivery, usually by caesarean section, unless the

second stage of labour is well advanced and rapid instrumental delivery is

possible.

It is important to note that even moving the mother to the operating room and

preparing for an emergency caesarean section should never preclude stepping

down in the event of improvement in the CTG and that this should be

communicated to the parents during the transfer process.

The historical rule of thumb for timing of intervention has been the ‘3-6-9-12’

rule (Figure 21.1). This has the advantage of being easily remembered in an

emergency and encouraging timely transfer to theatre in the event of a severe

prolonged deceleration; however, it does not encourage clinicians to consider

the underlying cause of acute hypoxia.

This can lead to overintervention in cases where the underlying cause could

have been reversed, increased maternal risks from rushed procedures and

unnecessary distress to mothers and partners. Failing to identify a cause of fetal

hypoxia may also lead to a failure to prepare the team for massive blood loss

associated with placental abruption or surgical complications associated with

uterine rupture. In these nonreversible causes of acute hypoxia, even 3 minutes

delay may lead to a difference in fetal condition at birth. It is important then to

first identify the cause of prolonged deceleration so that the rule is not

inappropriately applied.

In the absence of a nonreversible cause of acute hypoxia, over 90 per cent of

prolonged decelerations will recover by 6 minutes and 95 per cent within 9Figure 21.1 The '3,6,9,12,15' Rule.

minutes.9 This observation is the foundation of the 3-6-9-12 rule. As has

previously been discussed, in acute hypoxia it is expected that fetal pH will fall

at a rate of 0.01 per minute. Therefore, a fetus starting with a pH of 7.3 and no

other compromise would be expected to have a pH of 7.15 after 15 minutes and

7.0 after 30 minutes of continuous acute hypoxia.

The CTG may well show signs of recovery at 6 minutes – an attempt to return to

the baseline or an improvement in variability. In this case, with a normal

preceding CTG and with no nonreversible causes of hypoxia, it would be

reasonable to delay transfer to the operating room while continuing intrauterine

resuscitation (e.g. Figure 21.1). In the event of a continuing prolonged

deceleration, particularly with reducing variability, the 3-6-9-12 rule should be

applied, allowing for reassessment and change of plan at every stage until

operative delivery is actually commenced (Figure 21.2). In this situation, the

possibility of concealed abruption, an occult cord prolapse or an undiagnosed

scar dehiscence should be considered.Figure 21.2 CTG showing normal baseline variability in 3 minutes before deceleration and

in

the first 3 minutes of deceleration. The repetitive prolonged contractions caused by

syntocinon are the cause of deceleration, and at 6 minutes after syntocinon is stopped and

terbutaline has been administered, the baseline starts to recover to normal and is fully

recovered by 10 minutes. This patient was not transferred to theatre and the labour

continued to a normal delivery.

After the Prolonged Deceleration Has Resolved

In most cases, it is appropriate to continue with the labour; however, the whole clinical

picture should be carefully assessed before deciding to proceed. In the presence of

ongoing hypoxic changes on the CTG, particularly in the context of chorioamnionitis or

in the presence of meconium, it may be appropriate to consider delivery, especially if

there are concerns regarding the progress of labour. In general, if the features observed

on the CTG trace after recovery are similar to those seen before deceleration, it is

appropriate to continue labour.

When Is It Safe to Restart Oxytocin?

It is often the case that tachysystole occurs as the endogenous production of and

sensitivity to oxytocin increases as labour progresses and there may be no need to

restart exogenous oxytocin infusions. If augmentation with oxytocin is necessary in order

to continue the labour, there should be clear evidence of fetal well-being in the form ofnormal variability and a stable baseline before restarting an oxytocin infusion, and it

should be restarted at a lower infusion rate than that being used previously.

Suggested Approach to Management of

Prolonged Decelerations

1. Assess the patient for nonreversible causes while commencing conservative

measures. (If found deliver immediately)

2. Assess the CTG for features that predict recovery

3. Treat reversible causes – consider fluid administration, stop oxytocin and

consider acute tocolysis

4. Reassess the CTG and clinical picture

Management of Prolonged Decelerations

Figure 21.3

Management of Fetal BradycardiaA fetal bradycardia is a baseline value <110 bpm for >10 minutes. This could occur in

the setting of acute hypoxia that lasts for >10 minutes, in which case the onset would be

sudden and a cause would usually be identifiable and management would be as

described earlier. There are many other causes of a sustained baseline heart rate <110

bpm and careful consideration of these causes should be made if the CTG pattern is not

in keeping with an acute deceleration.

A FHR of 100–110 bpm may be normal, particularly in a postdates fetus. In this

case variability will be normal, accelerations are likely to be present and the baseline is

likely to be consistent with previous fetal heart measurements. No further intervention is

required and in fact if no other risk factors exist this is not an indication for continuous

EFM in labour.

Other causes for fetal bradycardia include placental transfer of maternal

medications, particularly beta-adrenoceptor blockers.10 Beta-blockers depress the

activity of the sympathetic nervous system that would normally tend to increase the

FHR. They may also be associated with a reduction in variability, however it would be

expected that the variability would not be entirely absent (often described as ‘pencil

tip’) and accelerations, while reduced in amplitude, would be expected to be present.

Fetal arrhythmias, particularly complete heart block, may appear on CTG as a

profound bradycardia. Congenital heart block is associated with a significant risk of

mortality but is rare, and the detailed management is out of the scope of this chapter. The

bradycardia in this case does not represent acute compromise, however over time the

lowered cardiac output and volume overload may cause myocardial damage, dilated

cardiomyopathy and impaired ventricular systolic function.11 The worst outcomes are

seen with rates <50–55 bpm.12 Diagnosis and delivery planning require assessment by a

fetal medicine specialist.

Common Pitfalls

Failure to identify underlying cause of prolonged deceleration/bradycardia is

the most common mistake made. As highlighted above, this may lead toinappropriate intervention, including major surgery on the mother and equally may

lead to a lack of preparation for serious obstetric emergencies.

Failure to use acute tocolysis when uterine hyperstimulation is the cause of fetal

hypoxia. In uterine hyperstimulation, one may well do a caesarean section and

deliver a baby with a cord pH of 7.01 and then may congratulate the team on a

disaster averted. Instead, an obstetrician should aim to be able to congratulate

himself/herself on achieving a normal delivery with normal gases and maintaining

one’s own blood pressure in the normal range by a simple administration of

terbutaline (to the mother) to treat uterine hyperstimulation so as to continue labour.

Failure to reassess the situation. Failure to stop a caesarean section when the

CTG has become reassuring is common and may lead to entirely unnecessary

surgery with significant consequences for the mother. Additionally, the fetus that is

delivered only minutes after recovering from a significant period of hypoxia is

likely to be in worse condition at birth than one with time to recover. Equally,

clinging to the hope that the CTG will recover after 10 minutes when there are no

signs of improvement is an unnecessary and dangerous delay for the fetus.

ExerciseFigure 21.4

1. A primigravida is induced at 41 + 5 weeks of gestation for postdates after a

normal pregnancy. The CTG up to this point has been entirely normal with a baseline

rate of 130 bpm and variability of 5–15 bpm. At 11:49, a deceleration begins and the

attending midwife appropriately moves the mother into the left lateral position.

You are called to the room at 11:54.

a. What are the first steps you would take to assess the patient?

b. What is the likely cause of this prolonged deceleration?

c. What would your management be?

d. What features on the CTG are reassuring?

e. What features on the CTG are concerning?

Now consider the trace again (Figure 21.5).Figure 21.5 CTG trace from 11:55 to 11:56.

f.

What phenomenon is demonstrated at 11:55–11:56?

g. Terbutaline is administered at 11:57. At 11:58 what would your next action be?

Figure 21.6 shows the full trace indicating first recovery of the baseline and second

restoration of normal variability suggesting an intact neurological system. The

tocograph clearly demonstrates that the uterine activity has been temporarily

abolished.

Figure 21.6 CTG trace after administration of terbutaline.

h. What might you expect to see next on the CTG?References

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