Pathophysiology of perinatal hypoxia (“birth asphyxia”)

If one does not understand the basic physiology of perinatal hypoxia (“birth asphyxia”) then resuscitation of the newborn, however many algorithms you learn, becomes a series of ritual interventions that may be difficult to remember under stress. However, once this physiology is known, the process can be easily understood and the appropriate actions of the resuscitator seem to be logical, predictable, and essentially very simple.

Before delivery, the baby's respiration occurs via the placenta. Immediately following delivery the baby has to fill its lungs with air while disposing of the fluid currently filling them and massively increase the circulation to the lungs in order to establish independent respiration. While preparing for this change, the baby undergoing vaginal delivery must also cope with intermittent obstruction of placental gas exchange during each uterine contraction. These intermittent obstructions can each last for around 90 s and will occur maybe four times every 10 min for the 30–60 min of the second stage of labor (in this stage of delivery, the baby is at greatest risk for severe hypoxia).

Animal experiments performed in the 1950s provide very useful information on the response of fetal mammals to acute hypoxia. The immediate fetal response to acute hypoxia is a rise in blood pressure, heart rate, and “breathing” movements. With continuing hypoxia the fetus becomes unconscious, breathing movements stop as higher breathing centers are disabled by hypoxia, and the heart rate rapidly falls as the fetus enters early terminal apnea.