When I was a pediatric resident in the early 1980s we used a mantra to guide our actions during any resuscitation effort: Air goes in and out, blood goes round and round, oxygen is good.
At the same time we knew oxygen affected arterial reactivity in at least two ways. First, inhaled atmospheric oxygen hastened transition from fetal to neonatal circulation after birth by decreasing pulmonary artery resistance and increasing ductus arteriosus resistance so blood would go to the lungs instead of make a shunt right-to-left through the foramen ovale directly into the left ventricle. Second, we learned empirically that if we decreased the fractional inhaled oxygen (FiO2) temporarily, umbilical artery catheter (UAC) placement or arterial blood gas (ABG) sampling was just that much easier.
Yet as pediatricians we also learned the hard way from our neonatal intensive care (NICU) rotations that supra-atmospheric oxygen concentration use–at least in preemies– had downsides. These manifested in an alphabet soup of complications we didn’t fully understand: retrolentil fibroplasia (RLF) later called retinopathy of prematurity (ROP), bronchopulmonary dysplasia (BPD), intraventricular hemorrhage (IVH), and the like.
There were probably other “oxygenopathies” we didn’t know we were inducing but at least folks were beginning to see they existed and could be mitigated or prevented, especially ROP. Because oxygen limits became de riguer in NICU circles–but also pediatric anesthesiology circles when surgical care was rendered–more damage may have been averted than anyone realized up until that time, in part because few ever questioned if “oxygen is good” outside of NICU settings.
