Intrapartum fetal surveillance

Chapter 10 Intrapartum fetal surveillance

David T Y. Liu, Mentors: Rosemary Buckley, Toby Fay

CHAPTER CONTENTS

Physiology and pathophysiology 73

Fetal heart rate: background 74

Further points 74

Fetal heart rate: types 75

Baseline FHR 75

Transient changes in heart rate 76

Transient acceleration 76

Early decelerations 76

Combined patterns – variable decelerations 76

Late decelerations 77

Fetal acid–base balance 80

Fetal blood sampling 81

Management of the abnormal fetal heart rate trace 82

Further points 82

Fetal acidaemia, Apgar scores and neurological outcome 82

Meconium and meconium aspiration 82

Management of meconium in amniotic fluid 83

Other considerations 83

Severe moulding 83

Fetal movements 83

Most babies deliver without problems. In complicated pregnancies, however, birth can be a hazardous process for the fetus. Intrapartum surveillance by manually assessing contractions and listening (60 seconds) at intervals (15 minutes in first stage, 5 minutes in second stage) to check the fetal heart rate is a well-established obstetric practice for uncomplicated pregnancies. Electronic instrumentation has been introduced to facilitate continuous intrapartum fetal monitoring (when auscultation suggests abnormality, when there is evidence of or potential fetal compromise). The fetus signals potential compromise by:

• alterations in heart rate

• the development of acidosis

• the passage of meconium

• the presence of excessive moulding

• excessive movements.

PHYSIOLOGY AND PATHOPHYSIOLOGY

The fetal cardiac output is controlled mainly by the heart rate rather than stroke volume. Cardiac output also varies with gestation. About half (50%) of the fetal cardiac output is directed to the low resistance placental circulation for oxygenation and nutrients. Flow rate in the umbilical vein is approximately 100 ml/kg per minute. The following statements are relevant to understanding intrapartum fetal surveillance:

• Normal fetal heart rate (FHR) is between 110 and 160 beats per minute. Vagal response slows the rate, for example during fetal head or cord compression, whereas in a healthy fetus sympathetic response or catecholamine release following anaemia, hyperthermia, sepsis or hypoxia will produce tachycardia up to a maximum of 220 beats per minute.

• A fetus with an intact brain and myocardium exhibits FHR accelerations of 15 beats per minute for more than 15 seconds above baseline recordings in response to fetal movements, tactile or auditory stimulation.

• The healthy fetus exhibits an intrinsic baseline FHR variability of 5–25 beats per minute. A ‘flat’ or ‘silent’ pattern with fewer than 5 beats per minute variability for 40 or less minutes can indicate fetal inactivity or fetal ‘sleep’.

• The fetus can improve myocardial oxygenation through a reflex compensatory mechanism or ‘diving reflex’ by slowing the heart rate during uterine diastolic. This mechanism can produce transient changes described as variable or late decelerations which in about 50% may signal the likely presence of metabolic acidaemia (normal umbilical artery pH 7.26 ± 0.08). Fetal blood sampling is required to differentiate between physiological or pathological heart rate responses.

• Umbilical vein compression causes a reflex vagal parasympathetic response and produces transient variable decelerations. Like late decelerations, persistent appearance of these patterns correlate with possible presence of fetal acidaemia.

FETAL HEART RATE: BACKGROUND

FHR can be recorded intermittently by auscultation with a Pinard stethoscope or electronically by a Doppler instrument. Doppler recordings rely on ultrasound registration of the Doppler shift to signal FHR. Continuous electronic FHR monitoring (Figure 10.1) was introduced to provide uninterrupted intrapartum recordings. A fetal scalp electrode and intrauterine pressure recordings were used to provide the described classic patterns of transient FHR changes. Intrapartum pressure recording of uterine activity, however, is now usually replaced by use of external transducers to register sequential changes in uterine contraction. Correct placement of this external contraction device is important. Idiosyncrasies between the intrauterine and external methods for recording uterine contraction must be appreciated. The universal principle of need to understand the workings of tools used must apply since FHR change is read against the peak of the displayed uterine contraction.

Figure 10.1 A machine used for continuous fetal heart rate monitoring.

Continuous electronic FHR monitoring is a screening adjunct for intrapartum fetal surveillance. Interpretation remains problematical and emphasises the need for constant education since failure to appreciate and react to signals of fetal insult is consistently identified as an avoidable factor in intrapartum fetal hypoxic damage or demise. Contemporary recommendation is that there should be an ongoing programme of education for interpretation of FHR changes for all involved in intrapartum care (Willis 2005).

Screening fetal welfare by recording FHR changes (cardiotocograms (CTGs)) should:

• interpret changes against a set of accepted definitions (for example, National Institute for Health and Clinical Excellence (NICE) 2001).

• interpret against the clinical presentation and background.

Further points

• Drugs, e.g. pethidine can blunt FHR responses whereas procedures such as insertion of an epidural block, vomiting, catheterisation and toileting can be followed by changes reflecting placental blood flow or vagal responses. Over 40% of fetuses in labour may show non-reassuring or abnormal traces. Discrepancy between fetal outcome, FHR and pH emphasises that non-reassuring FHR changes should be interpreted as a need for review and/or check fetal pH where appropriate. At best only 60–70% pathological changes are indicative of fetal acidaemia.

• There is intra- and inter-observer variation in interpretation. Attempts to standardise interpretation is thwarted by the lack of an internationally accepted guideline for interpretation and consensus for terminology or definition.

• A tocodynamometer essentially indicates only presence of a contraction. The peak of uterine contraction registered by an external tocometer need not equate with recordings from an intrauterine catheter. The peak of the contraction using an external tocodynamometer (photo) varies with the site of placement on the mother’s abdomen.

• There is no clear understanding of the relation between FHR changes and fetal myocardial or cerebral oxygenation.

• A normal CTG pattern reassures that only 2% of babies will have a pH of <7.25 at birth.

• A well-grown healthy fetus should withstand 90 minutes of hypoxic stress before the pH falls. Fetal reserve is less in a compromised fetus. The preterm fetus is more susceptible to hypoxia, in particular, damage of the type II pneumocytes. There is, however, no means to indicate how much hypoxic insult a healthy fetus can withstand.

• In 90% of cases of cerebral palsy the causative event occurs before onset of labour. In the remaining 10% intrapartum signs of hypoxia may reflect the presence of pregnancy compromise such as intrauterine growth restriction, fetal damage or infection.

• Usually hypoxaemia and metabolic acidaemia are progressive processes and timing of onset is difficult. Signs of fetal compromise are often insensitive and not specific to any particular cause.

• The fetus may be able to compensate until attendant effects of uterine contractions or strength of contractions produce added insult and threat of irreversible neurological damage.

• Fetal acidaemia may indicate ability of the fetus to respond appropriately to hypoxia. Metabolic acidaemia at birth is common (2%) and most of these babies do not develop neurological damage. Pathological acidaemia associated with increased risk of neurological damage is a pH <7.00 and a base deficit of >12 mmol/l. Existing fetal compromise must be kept in mind.

• The fetus is unlikely to be acidaemic if the FHR baseline is between 110 and 160 beats per minute, variability is within 5 and 25 beats per minute and there is no deceleration. Acidaemia is likely if there is bradycardia, no variability and persistent late or variable decelerations. In acute hypoxia the pH drops by 0.1 units/min.

• Fetal metabolic acidosis (pH <7.00 and base deficit of 12 mmol/l or more) is associated with increased risk of subsequent neurological deficit such as spastic quadriplegia.

• After 32 weeks the FHR patterns can be interpreted as for term babies. Before this gestation there are fewer accelerations and less than 20 second decelerations can occur spontaneously.

• Fetal sepsis is not usually associated with a low pH (pH <7.20) until the late stage of labour.

• A scalp electrode should not be used in women with the human immunodeficiency virus (HIV) or herpes simplex virus. Do not attach the clip to a fetus with a bleeding disorder, e.g. haemophilia.

FETAL HEART RATE: TYPES

During labour the FHR is described in terms of baseline rates (readings between contractions) and transient changes (readings during contractions). Four features – baseline rate, variability, presence of acceleration and deceleration – are used to assess fetal welfare.

Baseline FHR

• Normal – accepted as between 110 to 160 beats per minute recorded over 5 or 10 minutes (NICE 2001).

• Tachycardia – above 160 beats per minute. Sympathetic or catecholamine response. It is severe if above 180 beats per minute. Causes include maternal diseases such as infection and thyrotoxicosis; administered drugs, for example atropine, βsympathomimetics and hydralazine; fetal infection and hypoxia. A rate of between 161 and 180 beats per minute is non-reassuring.

• Bradycardia – below 110 beats per minute. Progressive or sudden slowing to less than 100 beats per minute suggests fetal decompensation. Known contribution by administered drugs such as opioids and local anaesthetics; fetal cardiac abnormalities, for example heart block and fetal hypoxia. A rate between 100 and 109 beats per minute is non-reassuring.

• Baseline variability – as a consequence of a fixed stroke volume, the FHR speeds and slows to maintain a stable blood pressure and cardiac output. Normally this variability is more than 5 beats per minute (distance between two faint horizontal score lines on recording paper) to 25 beats per minute. The term ‘flat trace’ or the electronic term ‘silent trace’ is used to describe variability of less than 5 beats per minute. The controlling centre for cardio-acceleration and deceleration is in the medulla. Variability is affected by:

• hypoxia – flat trace, sinusoidal patterns (smooth, sinewave pattern of 5–15 beats per minute recurring 3 to 5 times per minute lasting more than 10 minutes)

• depressant drugs, for example opioids, diazepam (flat trace)

• anaemia (sinusoidal patterns)

• machinery averaging techniques (display trace with less variability)

• neural tube abnormalities affecting control centre, e.g. anencephaly (flat trace)

• Doppler technique for FHR (produces a ‘noisy’ or irregular trace masking true variability).

• A flat trace for less than 20 minutes is nonreassuring or suspicious and is abnormal if the duration is longer than 20 minutes. Note fetal sleep pattern (up to 40 min). Interpret by considering all aspects, e.g. the trace of associated deceleration patterns.

Transient changes in heart rate

The fetus is subjected to compression and transient hypoxic stress during uterine contractions. Contractions above 4–6 kPa interrupt placental intervillous blood flow. The healthy fetus tolerates these impositions without much change in heart rate. With fetal compromise and/or non-physiological uterine contractions, patterns of transient FHR changes are observed reflecting the degree of fetal response. It takes 60–90 seconds for reoxygenation of the intervillous blood hence contraction intervals should not be less than 120 seconds.

Tags: Labour Ward Manual

Mar 16, 2017 | Posted by admin in NURSING | Comments Off

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