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.

Electronic fetal monitoring, cerebral palsy, and caesarean section: assumptions versus evidence

“…Firstly, fetal heart rate decelerations are commonly associated with peripheral chemoreflex rather than compression of the fetal head or umbilical cord, and may be relatively unthreatening. 15 Furthermore, studies consistently show that most cases of cerebral palsy in babies born at or near term are not caused by birth asphyxia but associated with congenital malformations, fetal growth restriction, intrauterine exposure to infection or inflammation, and other unknown factors. [11][12][13][14][15][16][17] A test that identifies abnormalities in a high percentage of births will inevitably produce a high false positive rate if used to identify an uncommon outcome such as cerebral palsy, guaranteeing an "arithmetic of failure."…”

Is the hypothesis that the commonest fetal heart rate decelerations are caused by peripheral chemoreflex due to fetal hypoxaemia correct?

“…This cannot be equated with the Cushing reflex – a sustained rise in intracranial tension in the rigid adult skull (Lear et al . ). Further support to refute head‐compression decelerations is sought from a clinical study (Walker et al .…”

“…) in which manual abdominal pressure over the fetal head reportedly provoked either decelerations or tachycardia (Lear et al . ). In this study manual pressure was applied in between contractions at five sites on the uterus from fundus down to the suprapubic area (fetal head) for 20–40 s causing a rise of intra‐amniotic pressure of about 100 mmHg.…”

“…This disproves the necessity of severe cerebral hypoperfusion and dangerous hypoxia during FHR decelerations from head compression, contrary to the assertion of Lear et al . ().…”

“…In the animal study quoted (Lear et al . ), the heads of fetal lambs were exteriorised from pregnant uterii, carotid vessels catheterised and fetal lamb heads were compressed with both hands (Paul et al . ).…”