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The purpose of monitoring the fetus in labour is to identify those who might be at increased risk of death or hypoxic injury so that delivery can be expedited and harm prevented. Fetal monitoring involves fetal heart rate (FHR) assessment, either by intermittent auscultation or by continuous electronic measurement (cardiotocography (CTG): ‘cardio’ meaning heart, ‘toco’ meaning labour). Intermittent auscultation of the fetal heart is appropriate for monitoring fetal condition in labours at ‘low risk’ of fetal hypoxia, with electronic fetal monitoring being advised in labours at increased risk (‘high risk’) of hypoxia or if concern is raised by preceding intermittent auscultation. A ‘normal’ CTG reliably identifies the non-hypoxic fetus, but the converse is not true regarding an ‘abnormal’ CTG; there is a high false-positive rate and many fetuses suspected to be hypoxic are not. As a consequence, the use of the CTG increases the rate of obstetric intervention in return for limited neonatal benefit.
The term ‘fetal distress’ is widely used to describe a clinical scenario in which there is concern regarding fetal well-being. Unfortunately, the term lacks a precise definition and its use is not encouraged. A standardised categorisation of the CTG enables a more meaningful way of communicating the magnitude of concern. Analysis of the electrocardiogram (ECG) waveform in association with the CTG can improve its ability to correctly identify hypoxia.
Fetal oxygenation depends on a number of factors.
During a contraction, the intramural vessels supplying the placenta are constricted by the smooth muscle fibres of the uterus. Provided that the contractions are not too long or too frequent, the placental blood supply has time to recover before the next contraction begins. In hyperstimulation, when the uterus is contracting too frequently, placental oxygenation may be impaired. In other circumstances, there may be placental hypoperfusion – for example, following the distal sympathetic blockade and associated hypotension – which can occur with spinal or epidural anaesthesia.
A small or poorly functioning placenta is less capable of adequate oxygen transfer than a larger or normally functioning placenta. In this situation, the fetus may already be growth restricted prior to the onset of labour and, therefore, more susceptible to hypoxic stress. In cases of placental abruption, partial placental separation leaves a reduced surface area for vascular communication. This results in less efficient oxygen exchange.
The fetus responds to hypoxia with peripheral vasoconstriction and redistribution of the blood to the heart and brain. Prolonged vasoconstriction may lead to damage in other organs manifesting in the neonatal period, such as the gastrointestinal tract (resulting in necrotising enterocolitis) and kidneys (renal impairment). Regardless of the protective effect of such redistribution, in the absence of intervention, prolonged or severe hypoxia and acidosis results in hypoxic brain damage or death.
Persistent or severe hypoxia leads to anaerobic metabolism and acidosis. The acid–base balance within the fetal circulation reflects the degree of oxygenation, which forms the basis of intrapartum fetal blood sampling (FBS).
FHR monitoring is recommended to all labouring women. The use of continuous electronic monitoring in ‘low-risk’ labours may increase the rate of intervention for little or no demonstrable benefit in terms of improved neonatal outcomes. It is important to consider which labours are at increased risk of hypoxia (so-called ‘high-risk’ labours) and which are ‘low risk’. Some of these factors are outlined in Box 32.1
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