16 Impact of Maternal Environment on Fetal Heart Rate. Handbook CTG

 16

Impact of Maternal Environment on

Fetal Heart Rate

◈

Ayona Wijemanne and Edwin Chandraharan

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

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

Introduction

The fetoplacental unit is a unique interface where oxygen is transferred to the fetus in

exchange for carbon dioxide and water. Oxygen transfer is dependent upon adequate

maternal oxygenation, uterine blood supply, placental transfer and integrity of the

umbilical cord. Disruptions to any of these can result in fetal hypoxia and a subsequent

change in fetal heart pattern on the CTG trace. Chemicals and inflammatory markers

associated with maternal conditions may also cross the placenta and cause changes in

fetal heart patterns. It is therefore important to consider the maternal environment when

interpreting a cardiotocograph (CTH).

Key Facts

Maternal conditions or factors that may affect fetal heart patterns can be broadly

categorized into the following groups:Conditions Causing Maternal Metabolic Acidosis

Conditions Causing Chronic Maternal Hypoxia

Conditions Reducing Placental Perfusion

This may lead to chronic hypoxia, as with:

Placental perfusion may also be reduced temporarily with the following conditions:

Maternal Autoantibodies

Diabetic ketoacidosis (DKA)

Uraemic acidosis secondary to renal failure

Starvation ketoacidosis

Alcoholic ketoacidosis

Maternal cardiovascular disease

Acquired/congenital cyanotic heart disease

Cardiac failure

Pulmonary hypertension

Chronic pulmonary disease

Cystic fibrosis

Severe maternal anaemia

Preeclampsia

Systemic lupus erythematosus

Maternal hypotension

Maternal tachyarrhythmia

Systemic lupus erythematosus

HyperthyroidismDrugs

Maternal Temperature

Sepsis has already been discussed separately. However, there have been several case

reports of maternal hypothermia (often resulting from sepsis) leading to prolonged

decelerations on the CTG. This is corrected by rewarming the mother. Similarly, a fetus

may react to maternal pyrexia by increasing its heart rate

Key Changes on the CTG Trace

Raised Baseline Fetal Heart Rate (FHR)

Reduced Baseline FHR

Reduced Variability

Opiates (e.g. pethidine)

Beta sympathomimetics (e.g. terbutaline)

Cocaine

Beta sympathomimetics (e.g. salbutamol or terbutaline)

Fetal hyperthyroidism secondary to maternal anti-TSH receptor antibodies

Congenital heart block secondary to maternal anti-Ro/La antibodies with SLE

(Systemic Lupus Erythematosus); a baseline bradycardia may be noted.

Chronic maternal hypoxia leading to chronic fetal hypoxic state

Severe maternal cardiac disease

Conditions resulting in reduced placental perfusion, leading to chronic fetal

hypoxic state

Opiates

Severe maternal metabolic acidosisChemoreceptor-Stimulated Decelerations

Prolonged Decelerations

Key Pathophysiology behind the Features

Observed on the CTG Trace

Raised Baseline FHR

Reduced Baseline FHR

Reduced Variability

Maternal metabolic acidosis

Maternal hypoglycaemia

Maternal hypotension

Maternal hypothermia

If present in significant titres, maternal anti-TSH receptor antibodies may cross

the placenta and cause neonatal thyrotoxicosis. This manifests as a fetal

tachycardia with a heart rate >160 bpm.

Beta sympathomimetics cross the placenta and stimulate the fetal sympathetic

nervous system, causing a fetal tachycardia.

Maternal anti-Ro (SSA) and anti-La (SSB) antibodies cross the placenta and, if

present in significant titres, cause inflammation of the fetal atrioventricular node

and myocardium, resulting in congenital heart block.

This occurs in 1–5 per cent of fetuses of mothers with SLE.

The baseline FHR will typically be <100 bpm; NICE guidelines will not apply

when interpreting such CTGs as this is a ‘nonhypoxic’ change in baseline FHR.Chemoreceptor-Simulated Decelerations

Prolonged Decelerations

Management

Management of CTG abnormalities involves two principles:

Chronic maternal hypoxia and conditions resulting in reduced placental

perfusion can cause intrauterine growth restriction and poor development of the

fetal autonomic nervous system.

Such fetuses will have reduced reserve and will not compensate for the hypoxic

stress of labour as healthy fetuses; that is, reduced variability will appear on the

CTG before the onset of decelerations and a rise in baseline.

Opiates depress the fetal autonomic nervous system, resulting in reduced

baseline variability.

Maternal acidosis can reduce uterine blood flow and lead to decreased

oxygenation of the fetoplacental unit. This change, along with the accumulation

of maternal hydrogen ions in the fetus, may lead to fetal acidosis and subsequent

reduced baseline variability. In these situations, variability may become reduced

before the onset of decelerations.

Maternal metabolic acidosis leads to an increased maternal hydrogen ion

concentration. These hydrogen ions cross the placenta and stimulate fetal

chemoreceptors, causing shallow decelerations on the CTG trace.

Maternal hypotension is most commonly caused by aortocaval compression.

Placental perfusion is reduced temporarily, causing a prolonged deceleration.

Correction of the precipitating cause

Relieving aortocaval compression by moving the mother into the left lateral

positionKey Tips for Optimizing the Outcome

Common Pitfalls

Warming the mother in cases of hypothermia

Considering the entire clinical picture

Threshold for delivery of growth-restricted fetuses will be much lower as

they have less physiological reserve.

Anticipate problems beforehand

Fetal cardiac surveillance in mothers with anti-Ro/La antibodies

Regular growth scans in mothers with medical conditions causing chronic

hypoxia

A thorough assessment of the mother’s medical condition on admission

Blood glucose and blood gas measurement in diabetic women with

suspected DKA (Diabetic Ketoacidosis)

A complete drug history including smoking and illicit drug use

Timely correction of the precipitating factor(s)

Anticipate a reactive fetal tachycardia for approximately 20 minutes after the

administration of a tocolytic (e.g. terbutaline) for uterine hyperstimulation, and

no intervention is necessary.

Proceeding directly to delivery by caesarean section in cases of prolonged

decelerations secondary to maternal conditions rather than correcting the

precipitating cause

Misreading a baseline bradycardia as a prolonged deceleration

Not considering the complete clinical pictureConsequences of Mismanagement

Exercise

1. A 31-year-old primigravida presents to the labour ward at 37 weeks of gestation with

a history of regular contractions. She was diagnosed with type 1 diabetes at the age of

11 and uses insulin pump therapy. Her HBA1c at booking was 56 mmol/mol and control

has been difficult during pregnancy. She appears dehydrated and urine dipstick shows

>3 ketones. On admission she is found to be 3 cm dilated and CTG monitoring is

commenced. The following trace is observed:

Figure 16.1

a. How would you classify the CTG?

b. What do you need to consider given her history and how might it impact upon the

CTG?

c. How will you manage her?

Unnecessary operative deliveries

Worsening of maternal medical condition (e.g. DKA) that, if left untreated, can

lead to maternal death

Worsening fetal outcomes as attempting to perform an emergency caesarean

section for a prolonged deceleration secondary to maternal hypotension may in

fact worsen fetal outcome while increasing unnecessary operative interventions

on the mother.Further Reading

1. Hutter D, Kingdom J, Jaeggi E. Causes and mechanisms of intrauterine hypoxia and its

imp

act on the fetal cardiovascular system: a review. Int J Paeds. 2010 (2010) 9.

2. Parker J, Conway D. Diabetic ketoacidosis in pregnancy. Obstet Gynaec Clin NA. 34

(2007) 533–543.

3. Aboud E, Neales K. The \effect of maternal hypothermia on the fetal heart rate. Int J

Obstet Gynecol. 66 (1999) 163–164.

4. Balucan F, Morshed S, Davies T. Thyroid autoantibodies in pregnancy: their role,

regulation and clinical relevance. J Thyroid Res. 2013 (2013) 15.

5. Jaeggi E, Laskin C, Hamilton R, Kingdom J. The importance of the level of maternal antiRo/SSA antibodies as a prognostic marker of the development of cardiac neonatal lupus

erythematosus. J Am Coll Cardiol. 55 (2010) 2778–2784.