The myths and physiology surrounding intrapartum decelerations: the critical role of the peripheral chemoreflex.
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.
The Fetal Physiology and Neuroscience Group, Department of Physiology, The University of Auckland, Auckland, New Zealand.
Christopher A
0000-0002-8937-0846
CA
Lear
The Fetal Physiology and Neuroscience Group, Department of Physiology, The University of Auckland, Auckland, New Zealand.
Robert
R
Galinsky
The Fetal Physiology and Neuroscience Group, Department of Physiology, The University of Auckland, Auckland, New Zealand.
Guido
G
Wassink
The Fetal Physiology and Neuroscience Group, Department of Physiology, The University of Auckland, Auckland, New Zealand.|Department of Obstetrics and Gynaecology, Mie University Graduate School of Medicine, Mie, Japan.
Kyohei
K
Yamaguchi
The Fetal Physiology and Neuroscience Group, Department of Physiology, The University of Auckland, Auckland, New Zealand.
Joanne O
JO
Davidson
The Fetal Physiology and Neuroscience Group, Department of Physiology, The University of Auckland, Auckland, New Zealand.|Department of Obstetrics and Gynaecology, The University of Auckland, Auckland, New Zealand.
Jenny A
JA
Westgate
The Fetal Physiology and Neuroscience Group, Department of Physiology, The University of Auckland, Auckland, New Zealand.
Laura
L
Bennet
The Fetal Physiology and Neuroscience Group, Department of Physiology, The University of Auckland, Auckland, New Zealand.|Starship Children's Hospital, Auckland, New Zealand.
Alistair J
0000-0003-0656-7035
AJ
Gunn
D000818:Animals; D001237:Asphyxia / Q000503:physiopathology; D017704:Baroreflex / Q000502:physiology; D005260:Female; D005333:Fetus / Q000502:physiology; D006257:Head / Q000502:physiology; D006340:Heart Rate, Fetal; D006801:Humans; D020896:Hypovolemia / Q000503:physiopathology; D007743:Labor, Obstetric; D011247:Pregnancy