Widespread use of fetal heart rate monitoring for intrapartum fetal surveillance preceded our detailed understanding of the behaviour and regulation of the fetal cardiovascular system during labour. The fetal heart rate is sensitive to fetal hypoxaemia and hypoxia, but lacks specificity for fetal acidosis, the end point of unmitigated hypoxaemia and hypoxia. Original interpretations of fetal heart rate patterns equated decelerations to ‘fetal distress’ and mandated operative intervention. Since then, obstetricians have been trained to focus on the morphological appearances of fetal heart rate decelerations rather than to understand the underlying physiological mechanisms, how the fetus compensates and defends itself, and those patterns that suggest progressive loss of compensation. Consequently, operative interventions are commonly undertaken to ‘rescue’ fetuses that display benign signs of fetal heart rate adaption to events in labour. Failure to recognise abnormal fetal heart rate patterns remains the leading cause of avoidable brain injury and litigation. In this chapter the general characteristics of the fetal heart rate, the changes in fetal heart rate pattern that may occur during labour, and the patterns that suggest failure of the fetal compensatory mechanisms leading to injury are discussed.
Basic principles of intrapartum fetal heart rate interpretation
Defining a normal or ‘near-normal’ cardiotocograph during labour
The clinical importance of a normal cardiotocograph (CTG) is that it establishes that the fetal neurological and cardiovascular systems are sufficiently intact and able to react and respond to defend the fetus against intrapartum insults. Secondly, it is the hallmark of a healthy fetus and symbolises fetal wellbeing, normoxia, normal fetal acid base status, absence of asphyxia and a low probability of developing intrapartum fetal asphyxia, barring some obstetric catastrophe. On the other hand, a ‘non-reactive’ fetal admission test is associated with adverse fetal outcome and long-term neurological deficit. It is reasonable to presume that a fetus with an abnormal CTG cannot be relied upon to display the predictable changes that characterise maladaptative responses to the asphyxiating process of labour; however, no direct evidence currently supports this.
A normal intrapartum CTG ( Fig. 1 ) should satisfy the following criteria: (1) it should have a stable baseline fetal heart rate (FHR) of between 110–160 bpm without decelerations; (2) it should have normal baseline FHR variability oscillating between 5–25 bpm above and below the stable baseline FHR; (3) it should also have periods of reduced FHR variability, which alternate with periods of increased FHR variability with or without accelerations, the fetal ‘cycling activity’.
In contrast to the antenatal period when the presence of accelerations is required to define a normal CTG, the absence of spontaneous FHR accelerations during labour is entirely acceptable provided that the other CTG features of fetal wellbeing are present. In practice, it is often possible to elicit FHR acceleration by stimulating the fetus.
Fetal cycling activity is the fundamental behavioural characteristic of the neurologically normal and non-hypoxic term or near term fetus. Collectively, these CTG features indicate normal fetal behaviour, neurological integrity, and the absence of significant hypoxia or acidosis. Although some obstetricians and midwives often worry unduly about normal and transient reduction in baseline FHR variability, a quantitatively normal or even increased FHR variability that does not alternate with a quiet period of reduced variability is not normal and should also elicit concern. Fetal cycling activity may be absent in hypoxia, chorioamnionitis, intrauterine fetal infection, exposure to drugs (including oxytocin, sedatives, narcotics, atropine), complete heart block, fetal brain haemorrhage, or malformation such as anencephaly.
Fetal heart rate decelerations
Put simply, an FHR deceleration is a reflex chemoreceptor-mediated parasympathetic response to a brief spell of oxygen deprivation (hypoxic, ischaemic stimulus, or both). It is widely believed that the purpose of this key adaptation is to reduce myocardial work load and oxygen demand. Most of the FHR decelerations (85% or more) observed during labour are variable decelerations, characterised by a sharp fall in FHR from the baseline, reaching the nadir in less than 30 s, and vary in depth, shape, duration and temporal relationship with contractions. Over the years, undue emphasis has been placed on these morphological appearances and the lack of relationship with contractions. In practice, however, these characteristics and emphasis do not add value to clinical interpretation or decision making. What matters is the fetal response to the stimuli that generate the decelerations. Early decelerations, as originally described by Hon and Quilligan and subsequently by Caldeyro-Barcia as ‘type 1 dips’ are exceedingly rare, and for practical purposes can be largely discounted. Because the so-called early decelerations or ‘type 1 dips’ were not associated with fetal acidosis, however, many clinicians extrapolated this to mean that decelerations that are synchronous with contractions are ‘early’ and are therefore benign, with disastrous consequences. Late decelerations lag behind uterine contractions in timing and are caused by impaired oxygen transfer across the placenta. The relevant clinical question to ask whenever decelerations emerge in a previously normal CTG is whether the fetus is compensating appropriately and adequately to the cause(s) and the effects of the decelerations. The answer to this critical question is at the centre of appropriate interpretation and application of intrapartum FHR monitoring.
The healthy fetus with a previously normal CTG will display a predictable set and sequence of FHR changes in response to hypoxic ischaemic insults, depending on whether these are slow in onset, mild to moderate and progressive, or acute and profound. The qualitative patterns of these responses are predictable and should form the template for effective and clinically meaningful FHR interpretation.
Fetal heart rate variability
The FHR variability may be defined as random fluctuations in the baseline FHR, which are irregular in amplitude and frequency. These fluctuations are induced by the abrupt but normal changes in the interval between consecutive heart beats. In clinical practice, FHR variability is assessed visually and quantified as the amplitude of peak-to-trough in beats per minute. The origin of the FHR variability is complex, with inputs from other cycling physiological systems. The fetus requires integrity of the cerebral cortex, midbrain, vagus nerve, and the cardiac conductive tissues to exhibit normal FHR variability. The fetus with a normal FHR variability is at a low risk of immediate death or brain injury caused by asphyxia, regardless of the presence of decelerations or bradycardia. On the other hand, a reduction or absence of FHR variability was reported to be an important indicator of fetal hypoxia and evolving acidaemia in term and preterm fetuses. A recent systematic review suggested that the most consistent predictor of newborn acidaemia was minimal or undetectable FHR variability, although animal experiments have also shown increased FHR variation with the onset of severe acidosis and hypotension in one-third of term-equivalent fetal sheep subjected to repeated brief umbilical cord occlusions.
A number of key clinical conclusions may be drawn from the above discussions: (1) during labour, and in the presence of FHR decelerations, intermittent or sustained reductions in FHR variability may signal the onset of decompensation, unless fetal asphyxia could be excluded; (2) in the presence of normal FHR variability, the role of fetal blood sample is limited ; (3) a fetus with a previously normal FHR variability will not switch to one with reduced or absent variability without the input of asphyxial FHR decelerations; (4) if the FHR variability is absent at the outset of monitoring, then it is impossible to distinguish between asphyxial and non-asphyxial causes of decreased FHR variability without determination of fetal acid base status.
Fetal cardiovascular responses to intrapartum oxygen deprivation
As the constant supply of oxygen is essential for the production of cellular energy and maintenance of cellular integrity (in essence for life itself), the cardiovascular system is programmed to rapidly detect, assess, and redress any form of oxygen deprivation. The sole aim of this response is the centralisation of the circulation to maintain perfusion of the essential organs the brain, the myocardium, and the adrenals at the expense of the non-essential organs, such as the lungs, skin, muscles, liver, kidneys, and the gastrointestinal tract. The response is initiated by the rapid response neural chemoreflexes in the immediate to short term, and subsequently augmented by the slower acting endocrine, endothelial and behavioural responses in the medium to long term. Once activated, the chemoreflex response is qualitatively similar but quantitatively different across insult paradigms, and is finely calibrated to produce varied responses, depending on the severity of the insult and the cellular tolerance of the host.
Hypoxic insults that are slow in onset and persistent over time allow the fetus to make homeostatic adaptations, including metabolic adjustments, and elicit different FHR patterns. Experimental studies in fetal sheep have shown that the fetus can sustain its protective cardiovascular system adaptations during prolonged hypoxaemia in the absence of progressive metabolic acidaemia. These protective adaptations begin to fail with the development of acidaemia; at pH less than 7.0, the entire fetal and cerebral oxygen consumption fall substantially. Acidaemia leads to loss of vascular tone, cardiac cell injury, depressed myocardial function, and hypotension with resultant ischaemic brain injury ( Fig. 2 ). On the other hand, Clapp et al. showed that significant neurological injury can be produced in the sheep model with intermittent cord compression, irrespective of acidosis or encephalopathy. Within the brain, regional distribution of flow shunts blood away from the cortex to the deep nuclei and brain-stem structures. In contrast, during total profound asphyxia (e.g. massive abruption, total cord occlusion or uterine rupture) fetal pO 2 rapidly reduces within minutes, resulting in an initial rapid chemoreflex-mediated generalised vasospasm, followed by hypoxic decompensation and finally profound systemic hypotension and brain infarction in such quick successions that regional redistribution of blood within the brain is unsuccessful in protecting the deep structures. In the dramatic cases the reduced cardiac output and hypotension result in such profound and prolonged FHR deceleration, that circulatory centralisation and regionalisation of blood flow within the brain fail, leading to injuries in the vulnerable regions of the brain before other systemic organs.
Fetal cardiovascular responses to intrapartum oxygen deprivation
As the constant supply of oxygen is essential for the production of cellular energy and maintenance of cellular integrity (in essence for life itself), the cardiovascular system is programmed to rapidly detect, assess, and redress any form of oxygen deprivation. The sole aim of this response is the centralisation of the circulation to maintain perfusion of the essential organs the brain, the myocardium, and the adrenals at the expense of the non-essential organs, such as the lungs, skin, muscles, liver, kidneys, and the gastrointestinal tract. The response is initiated by the rapid response neural chemoreflexes in the immediate to short term, and subsequently augmented by the slower acting endocrine, endothelial and behavioural responses in the medium to long term. Once activated, the chemoreflex response is qualitatively similar but quantitatively different across insult paradigms, and is finely calibrated to produce varied responses, depending on the severity of the insult and the cellular tolerance of the host.
Hypoxic insults that are slow in onset and persistent over time allow the fetus to make homeostatic adaptations, including metabolic adjustments, and elicit different FHR patterns. Experimental studies in fetal sheep have shown that the fetus can sustain its protective cardiovascular system adaptations during prolonged hypoxaemia in the absence of progressive metabolic acidaemia. These protective adaptations begin to fail with the development of acidaemia; at pH less than 7.0, the entire fetal and cerebral oxygen consumption fall substantially. Acidaemia leads to loss of vascular tone, cardiac cell injury, depressed myocardial function, and hypotension with resultant ischaemic brain injury ( Fig. 2 ). On the other hand, Clapp et al. showed that significant neurological injury can be produced in the sheep model with intermittent cord compression, irrespective of acidosis or encephalopathy. Within the brain, regional distribution of flow shunts blood away from the cortex to the deep nuclei and brain-stem structures. In contrast, during total profound asphyxia (e.g. massive abruption, total cord occlusion or uterine rupture) fetal pO 2 rapidly reduces within minutes, resulting in an initial rapid chemoreflex-mediated generalised vasospasm, followed by hypoxic decompensation and finally profound systemic hypotension and brain infarction in such quick successions that regional redistribution of blood within the brain is unsuccessful in protecting the deep structures. In the dramatic cases the reduced cardiac output and hypotension result in such profound and prolonged FHR deceleration, that circulatory centralisation and regionalisation of blood flow within the brain fail, leading to injuries in the vulnerable regions of the brain before other systemic organs.
Intrapartum cardiotogograph patterns associated with fetal hypoxia and neurologic injury
During labour, an intact fetus with a previously normal CTG will inevitably exhibit a predictable sequence of FHR responses after the emergence of hypoxic ischaemic insults, depending on the nature and severity. The patterns of these FHR responses are reliable predictors of the patterns of potential brain injury that may result if they were allowed to persist. Four distinct patterns of intrapartum hypoxia are commonly encountered during labour, namely slowly evolving hypoxia; subacute hypoxia; acute hypoxia; and chronic (or pre-existing) hypoxia. It is my firm belief that recognition of these patterns is essential to effective management and the prediction of the resultant brain injury. In some instances, there may be dual insults, which may be sequential with characteristic overlapping injury types.
Slowly evolving hypoxia
With a normal CTG, the onset of intermittent episodes of oxygen deprivation or hypoxaemia results first of all in the appearance of decelerations associated with uterine contractions ( Fig. 3 a and b). The amplitude and duration of the decelerations depend on the severity and duration of the hypoxic stress or insult. During labour, this is usually caused by cord compression, and sometimes may follow injudicious use of oxytocin. Persistence or more likely progression of these insults results in a second change in the CTG manifested as an increase in the baseline FHR, usually to about 160–180 bpm ( Fig. 3 c) as the baby increases his cardiac output via an adrenaline surge to deal with the stressful stimuli. Unlike adults, the fetus cannot increase its stroke volume significantly, and therefore relies almost entirely on raising its FHR to increase its cardiac output. Therefore, a sustained FHR tachycardia in association with uterine contractions is a sensitive marker of a compensatory increase in fetal cardiac output ( Fig. 3 c and d). It is widely believed that the fetal cardiac output does not change in the absence of significant acidaemia.
The duration of time that babies can spend at their maximum FHR without damage is variable, and depends on the individual baby’s reserve. Fleischer et al. showed that, in well-grown term fetuses in spontaneous labour with clear liquor and a previously reactive CTG, the average time taken for 50% of them to develop acidosis depended on the type of decelerations present, and was 115 mins with repeated late decelerations, 145 mins with variable deceleration, and 185 mins with flat and non-variable trace. Needless to say, that these threshold times do not apply to fetuses with reduced physiological reserve, including intrauterine growth restriction, thick meconium, or infection, and that acidosis may develop earlier. The critical factor here is that slowly evolving hypoxia is gradual in onset and allows the fetus time to make cardiovascular system and metabolic adjustments and that, in the absence of progressive metabolic acidaemia, the fetus can sustain its protective circulatory adaptations almost indefinitely. As outlined above, however, these protective adaptations will begin to fail with the development of acidaemia. At birth, the baby, subjected to slowly evolving hypoxia, is likely to exhibit signs of multi-organ dysfunction, including abnormal liver and kidney function consistent with the longstanding withdrawal of blood flow to these organs to protect the essential organs from hypoxia.
The third CTG abnormality to be observed if the noxious stimulus was not removed is reduction or lack of baseline variability ( Fig. 3 d and e). Finally, as the fetal myocardium begins to tire from the persistent lack of oxygen, the FHR falls gently towards a terminal bradycardia ( Fig. 3 e and f). Well-grown, normal, term fetuses in spontaneous labour with clear liquor and a previously normal CTG would take at least 1 h to transit through and display these changes.
Subacute hypoxia
Subacute hyoxia is characterised by complicated variable decelerations, with the amplitude of the deceleration 60 bpm or more and lasting for 90 s or more. When the baby’s FHR returns to its baseline, it spends less than 60 s before the onset of the next deceleration ( Fig. 4 a–d). The brief duration of time spent at the baseline FHR during recovery is insufficient to rid the fetus of its CO 2 burden accumulated during the preceding deceleration lasting 90 s or more. Therefore, a rapidly cumulative build up of CO 2 takes place and initially respiratory but subsequently metabolic acidosis. The actual baseline FHR may be within the normal range of 110–160 bpm, as the fetus is unable to raise its baseline FHR because of the brief time at the baseline after recovery before the onset of the next deceleration. Subacute hypoxia is associated with a rapid decline in pH, usually at the rate of 0.01 every 2–4 mins, in contrast to the slowly evolving hypoxia process where the rate of fall of the pH is usually much more slowly.
