The myths and physiology surrounding intrapartum decelerations: the critical role of the peripheral chemoreflex

Abstract

A distinctive pattern of recurrent rapid falls in fetal heart rate, called decelerations, are commonly associated with uterine contractions during labour. These brief decelerations are mediated by vagal activation. The reflex triggering this vagal response has been variably attributed to a mechanoreceptor response to fetal head compression, to baroreflex activation following increased blood pressure during umbilical cord compression, and/or a Bezold-Jarisch reflex response to reduced venous return from the placenta. Although these complex explanations are still widespread today, there is no consistent evidence that they are common during labour. Instead, the only mechanism that has been systematically investigated, proven to be reliably active during labour and, crucially, capable of producing rapid decelerations is the peripheral chemoreflex. The peripheral chemoreflex is triggered by transient periods of asphyxia that are a normal phenomenon associated with all uterine contractions. This should not cause concern as the healthy fetus has a remarkable ability to adapt to these repeated but short periods of asphyxia. This means that the healthy fetus is typically not at risk of hypotension and injury during uncomplicated labour even during repeated brief decelerations. The physiologically incorrect theories surrounding decelerations that ignore the natural occurrence of repeated asphyxia probably gained widespread support to help explain why many babies are born healthy despite repeated decelerations during labour. We propose that a unified and physiological understanding of intrapartum decelerations that accepts the true nature of labour is critical to improve interpretation of intrapartum fetal heart rate patterns.

Figure 1. Relationship between mean arterial pressure (MAP, mmHg), fetal heart rate (FHR, beats min ⁻¹ (bpm)) and changes in cerebral oxygenated haemoglobin (μmol (100 g) ⁻¹ ), as measured by near‐infrared spectroscopy, during a prolonged complete umbilical cord occlusion in a near‐term fetal sheep (0.85 of gestation)

The period of occlusion is shown in light grey. The overlapping dark grey area represents the initial and most rapid portion of the deceleration. Note how both FHR and cerebral oxygenated haemoglobin begin to fall in parallel at 6 s after the start of occlusion when MAP is not markedly higher than baseline. Data are 1 s averages. Cerebral oxygenated haemoglobin is shown relative to the average of the 2 min baseline period.

Figure 2. Fetal heart rate (FHR, beats min ⁻¹ (bpm)) and mean arterial pressure (MAP, mmHg) during three successive 1 min complete umbilical cord occlusions, repeated every 5 min in a near‐term fetal sheep (0.85 of gestation)

The periods of occlusion are shown in grey. Note that the major actively mediated increase in MAP is delayed until after the onset of decelerations. Additionally the release of occlusion is not associated with the development of hypotension below baseline levels. The first occlusion shown here is the 18th in a series of 49 occlusions; at this time arterial pH was 7.358, with a lactate of 1.6 mmol l⁻¹. Data are 1 s averages.

Figure 3. Cardiovascular responses during spontaneous uterine contractions in a near‐term fetal sheep (0.85 of gestation)

Fetal heart rate (FHR beats min⁻¹ (bpm)), mean arterial pressure (MAP, mmHg) and amniotic pressure (mmHg) during uterine contractions resulting in a deep deceleration (left panels) and multiple moderate decelerations (right panels). Labour was induced by the administration of betamethasone (11.4 mg, i.m. to the ewe x2, 24 h apart) as previously described (Liggins, 1969). Contractions began approximately 48 h after the first dose of betamethasone. Note in the left panels that the deep deceleration occurred despite an initial mild fall in MAP at the start of contraction while delayed hypertension develops late in the deceleration, consistent with the data presented in Figs 1 and 2 during complete umbilical cord occlusion. Only the second to last contraction in the right panels was associated with an increase in MAP at the start of the deceleration. Thus the baroreflex cannot be a consistent trigger of decelerations. Data are 1 s averages.

Figure 4. Factors that influence fetal oxygenation over the course of an intrapartum uterine contraction

During the course of an individual contraction, there is a critical balance between factors promoting a fall in fetal arterial oxygenation and those that sustain it – the relative strengths of these factors will determine the extent to which fetal arterial oxygenation falls during an individual contraction. Greater strength and duration of a uterine contraction leads to greater impairment of gaseous exchange, while antenatal factors such as impaired utero‐placental perfusion can exacerbate the severity of fetal deoxygenation. Fetal oxygen extraction must continue during a uterine contraction; however, the fetus can adapt to this reduced gas exchange by reducing non‐vital metabolic and behavioural processes, and so reduce its oxygen consumption. The degree to which fetal oxygenation falls during a contraction will determine the magnitude of the peripheral chemoreflex response, and, in turn, the depth of any resulting deceleration.

Figure 5. Factors that influence fetal anaerobic reserve and fetal oxygen debt during labour

Periods of brief asphyxia are frequent and a normal component of labour. This is offset by the fetus’ ability to adapt to these challenges through peripheral chemoreflex activation and a high anaerobic tolerance. Thus, the vast majority of fetuses adapt effectively to labour and are born healthy. The ability to adapt is finite, however, and can fail in two situations. Firstly, a fetus with good antepartum health and adequate anaerobic reserves can progressively decompensate if exposed to severe repeated asphyxial challenges that are too frequent to allow complete recovery between intense uterine contractions. Secondly, and perhaps of more clinical importance, is the scenario of a fetus entering labour with poor utero‐placental exchange capacity and reduced glycogen reserves. Such fetuses are unable to fully compensate to the repeated asphyxial challenges of a typical labour and will quickly decompensate, leading to hypotension and increasing risk of neural injury.