10 Role of Uterine Contractions and Intrapartum Reoxygenation Ratio. Handbook CTG

 10

Role of Uterine Contractions and

Intrapartum Reoxygenation Ratio

◈

Sadia Muhammad 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

The frequency, duration and strength of uterine contractions should be

considered whilst interpreting Cardiotocograph.1-3 During labour, uterine

contractions compress spiral arteries and thereby interrupt blood flow to

intervillous space leading to a reduction in placental perfusion.4–6 Intrauterine

pressure during labour may reach 85–90 mm Hg, and this is further elevated with

maternal pushing. The Ferguson reflex at full dilatation of cervix further releases

oxytocin, which increases the strength, frequency and duration of contractions

affecting further gaseous exchange during second stage of labour.

The onset of maternal pushing (active second stage of labour) decreases

maternal oxygenation leading to a reduction in the oxygenation of placental

venous sinuses and thereby further increasing the risk of acidaemia with higher

levels of lactic acid and CO₂. Uterine hyperstimulation secondary to the use of

oxytocin infusion during second stage of labour may further increase the risk of

acidaemia as further reduction in utero-placental perfusion.5Key Features (Increased Uterine Activity)

An Acute Increase in Uterine Activity (e.g. Immediately after Increasing

Oxytocin Infusion)

Most healthy fetuses cope with ongoing stress of labour without sustaining any

hypoxic injury and are vigorous at birth. However, the use of uterotonics for

induction or augmentation of labour leads to an increase in uterine activity.

Scientific research suggests that when uterine contractions occur at intervals of

<2 to 3 minutes, there is an increased likelihood of diminution of blood flow to

intervillous space. If this is repeated, intermittent interruption of fetal

oxygenation exceeds a critical level, then fetal decompensation may ensue and

progression from hypoxaemia to hypoxia, acidaemia to acidosis and even

asphyxia and resultant abnormal FHR pattern may occur.7

Research comparing the effect of excessive uterine activity on the fetal oxygen

saturation using near–infra red spectrometry concluded that fetal cerebral oxygen

saturation reached the lowest level of 92 seconds after the peak of contraction

with approximately 90 seconds to return to original baseline level.8 In addition,

an incomplete recovery to baseline was observed when uterine contractions

occurred once in every 2 minutes and fetal oxygen saturation decreased

incrementally after each contraction recovering only after oxytocin was stopped.

A more recent study by Bakker et al.9 concluded that five or more contractions in

10 minutes during second stage of labour was associated with a higher incidence

of neonatal acidaemia at birth when compared with contractions that were less

frequent.

A recent pilot study at St George’s University Hospitals NHS Foundation Trust

has shown that lower intrapartum reoxygenation ratio (<1) was associated with a

‘pathological CTG’ at the time of active second stage of labour (Figure 10.1).

The average reoxygenation ratio in fetuses with Apgar scores <5 was lower

(reoxygenation ratio <1) at both 1 and 10 minutes as compared to fetuses that had

Apgar score >5.10Effects of Continuing Increase in Uterine Activity over Time

Figure 10.1 Intrapartum reoxygenation ratio (‘x’ divided by ‘y’).

Key Pathophysiology behind Patterns Seen on

the CTG Trace

Prolonged deceleration refers to a sudden drop in baseline heart rate (<110 bpm

and usually <80 bpm). This may be short-lasting (up to 3 minutes) or prolonged

(3–10 minutes).

Baseline bradycardia refers to a baseline FHR <80 bpm persisting >10 minutes

Variable decelerations become more frequent, wider, and deeper – leading to an

‘atypical’ pattern.

Disappearance of accelerations.

Late decelerations (utero-placental insufficiency leading to acidosis).

Baseline tachycardia (catecholamine surge), reduced baseline variability and

stepladder pattern leading to bradycardia.

Physiologically, the frequent compression of uterine spiral arterioles without

adequate relaxation time would result in diminished placental perfusion and

impaired delivery of oxygen to the fetus, increasing the likelihood of fetal

hypoxia and acidosis.Recommended Management

Utero-placental insufficiency during labour results in the accumulation of carbon

dioxide and hydrogen ions due to fetal metabolic acidosis that occurs secondary

to anaerobic metabolism in the fetus.

Increased carbon dioxide and hydrogen ion concentration coupled with

decreased oxygen content of the fetal blood would stimulate the chemoreceptors,

resulting in the activation of the parasympathetic component of the autonomic

nervous system leading to a fall in the fetal heart.

Chemoreceptor-mediated deceleration takes a longer time to recover because

fresh oxygenated blood from the mother has to ‘wash out’ the accumulated acid

and carbon dioxide after the cessation of a uterine contraction. Therefore, this

results in a ‘lag time’ for FHR to recover back to its original baseline.

As a fetus descends into maternal pelvis during the second stage of labour, it gets

compressed leading to raised fetal intracranial pressure. Stimulation of the dura

mater, which is richly supplied by the parasympathetic nervous system, leads to

‘early’ decelerations in the CTG trace.

If CTG abnormalities secondary to increased uterine activity are observed,

oxytocin infusion should be immediately stopped (acute prolonged deceleration

or loss of baseline FHR variability) or reduced (recurrent decelerations with

stable baseline FHR and reassuring variability) based on the CTG abnormality.

Abdominal examination to assess uterine activity (uterine tone, duration and

frequency of contractions) and a vaginal examination to exclude an umbilical

cord prolapse, rapid cervical dilatation, placental abruption and uterine scar

dehiscence in case of previous caesarean sections should be performed. A fetal

scalp electrode may be considered in the absence of ‘acute intrapartum

accidents’.

Maternal blood pressure and pulse rate should be checked to exclude maternal

hypotension.Pearls

Pitfalls

Pitfalls include failure to appreciate the effect of cumulative ‘uterine activity’ on the

fetus and merely concentrating on the frequency of uterine contractions, as there is no

clear information regarding cumulative uterine activity in most international guidelines.

Intrauterine resuscitation (changing maternal position, administration of

intravenous fluids – a 500 mL bolus of Hartmann solution) should be attempted.

In cases of uterine hyperstimulation not resolving with initial measures, tocolysis

(terbutaline 250 mcg subcutaneously) should be considered.

Assess for recovery of fetal heart and a decrease in uterine activity, and, in the

absence of acute intrapartum accidents, if the ongoing prolonged deceleration on

the CTG trace does not recover by 9 minutes, then delivery should be expedited.

Early recognition of uterine hyperstimulation is crucial as poor utero-placental

perfusion can result in impaired fetal perfusion and subsequent fetal

compromise.

Caution should be exercised while increasing the dose of oxytocin infusion

because the uterine myometrium becomes progressively more sensitive to

circulating oxytocin due to the formation of oxytocin receptors on the fundus of

the uterus with advancing labour.

ACOG has defined tachysystole as over six contractions in a 10-minute window

averaged >30 minutes. Based on fetal oxygenation studies, researchers have

suggested to redefine this definition as over six in a 10-minute period with the

possibility of decreased fetal oxygenation due to inadequate relaxation time

between contractions. However, with the use of oxytocin, even three to four

contractions may result in fetal hypoxic-ischaemic injury.Consequences of Mismanagement

Exercises

1. A 25-year-old primigravida at 39 weeks of gestation presented with a history of

spontaneous onset of labour. On vaginal examination, her cervix was 6 cm dilated

with the presence of grade 2 meconium staining of the amniotic fluid.

Four hours later, her labour was augmented with syntocinon (oxytocin) infusion

as there was no progress of labour, and ongoing uterine contractions were deemed

inadequate.

Two hours after commencement of syntocinon infusion, uterine contractions were

occurring 6 in 10 minutes each lasting 60 seconds on the CTG trace (Figure 10.2).

Failure to take immediate measures to improve utero-placental circulation when

evidence of fetal decompensation (loss of baseline variability or sudden

prolonged deceleration) is observed. In such cases, in addition to stopping

oxytocin infusion (or removal of prostaglandin pessary), tocolytics should be

administered to improve utero-placental circulation.

Mismanagement in second stage of labour can result in rapid development of

fetal hypoxia, fetal decompensation and hypoxic injury leading to hypoxicischaemic encephalopathy.

Failure to understand the pathophysiological changes behind features observed

on the CTG trace may result in unnecessary surgical intervention with associated

morbidity.

Intrapartum fetal death or early neonatal death.

Fetal hypoxic injury due to uterotonics is very difficult to defend from a medicolegal point of view as this is iatrogenic and preventable.Figure 10.2

a. What is your differential diagnosis?

b. Is CTG monitoring indicated?

c. What abnormalities will be noted on the CTG based on the differential

diagnosis?

d. What is your management?

e. What will be noticed on the CTG trace if treatment is instituted?

References

1. Rooth G, Huch A, Huch R. Guidelines for the use of fetal monitoring. Int J Gynecol

Obstet. 1987; 25: 159–67.

2. Clinical Effectiveness Support Unit. The use of electronic fetal monitoring: The use of

cardiotocography in intrapartum fetal surveillance. Evidence-based clinical guideline number

8. London: RCOG Press; 2001.

3. ACOG Technical Bulletin. Fetal heart rate patterns: monitoring, interpretation, and

management. Int J Gynecol Obstet. 1995; 51: 65–74.

4. Uterine contraction monitoring. In: Freeman RK, Garite JY, Nageotte MP, eds. Fetal

heart monitoring, 3rd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2003, pp. 54–62.

5. Fleisher A, Anyaegbunum AA, Schulman H, Farmakides G, Randolph G. Uterine and

fetal umbilical artery velocimetry during normal labor. Am J Obstet Gynecol. 1987; 157: 40–3.6. Brar HS, Platt LD, Devore GR, Horenstein J, Madearis AL. Qualitative assessment of

maternal and fetal umbilical artery blood flow and resistance in laboring patients by Doppler

velocimetry. Am J Obstet Gynecol. 1988; Apr; 158(4):952–6.

7. American College of Obstetricians and Gynaecologists, American Academy of Pediatrics.

Neonatal encephalopathy and cerebral palsy: Defining the pathogenesis and

pathophysiology. Washington, DC: ACOG and AAP; 2003.

8. McNamara H, Johnson N. The effect of uterine contractions on fetal oxygen saturation. Br

J Obstet Gynaecol. 1995; 102: 644–7.

9. Bakker PCAM, Kurver PHJ, Kuik DJ, et al. Elevated uterine activity increases the risk of

fetal acidosis at birth. Am J Obstet Gynecol. 2007; 196: 313e1–313.e6.

10. Muhammad S, Lowe V, Chandraharan E. Correlation between intrapartum re-oxygenation

ratio and observed abnormalities on the CTG trace. Singapore J Obstet Gynaec. 2013; 44:

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