Abstract
Cerebrovascular pressure autoregulation promotes stable cerebral blood flow (CBF) across a range of arterial blood pressures. Cerebral autoregulation (CA) is a developmental process that reaches maturity around term gestation and can be monitored prenatally with both Doppler ultrasound and magnetic resonance imaging (MRI) techniques. Postnatally, there are key advantages and limitations to assessing CA with Doppler ultrasound, MRI, and near-infrared spectroscopy. Here we review these CBF monitoring techniques as well as their application to both fetal and neonatal populations at risk of perturbations in CBF. Specifically, we discuss CBF monitoring in fetuses with intrauterine growth restriction, anemia, congenital heart disease, neonates born preterm and those with hypoxic-ischemic encephalopathy. We conclude the review with insights into the future directions in this field with an emphasis on collaborative science and precision medicine approaches.
Highlights
Cerebral autoregulation (CA) is the physiologic adaptation in cerebrovascular resistance across a range of cerebral perfusion pressure (CPP; typically estimated using mean arterial pressure, MAP) in order to promote stable cerebral blood flow (CBF)
These experiments effectively replicate in the human fetus, those classic studies in the chronically instrumented pregnant ewe that form the basis for our current understanding of fetal and placental hemodynamics [39,40,41,42]
Traditional methods of CBF monitoring facilitated our foundational understanding of the maturational process of these complex mechanisms and their behavior in the setting of perturbed hemodynamics
Summary
Cerebral autoregulation (CA) is the physiologic adaptation in cerebrovascular resistance across a range of cerebral perfusion pressure (CPP; typically estimated using mean arterial pressure, MAP) in order to promote stable cerebral blood flow (CBF). Low fetal CPR is associated with high uterine artery Doppler indices and is thought to be a consequence of impaired placental perfusion that increases the risk for stillbirth [31] It may result from cerebrovascular vasodilation, which is common in fetuses growing poorly and is discussed further in the section on intrauterine growth restriction (IUGR). Using advanced MR imaging techniques that combine fetal cardiac MRI with T2 mapping to determine tissue oxygen saturations have enhanced our understanding of fetal circulation [38] These experiments effectively replicate in the human fetus, those classic studies in the chronically instrumented pregnant ewe that form the basis for our current understanding of fetal and placental hemodynamics [39,40,41,42]. Using NIRS to estimate CBF relies on the assumptions that the overwhelming majority of oxygen in blood is bound to hemoglobin, total hemoglobin is proportional to cerebral blood volume, and there is uniform
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