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Cerebral Hemodynamics in Premature Infants
Journal article   Open access   Peer reviewed

Cerebral Hemodynamics in Premature Infants

Christopher J. Rhee, Danielle R. Rios, Jeffrey R. Kaiser and Ken Brady
Neonatal medicine (Seoul, Korea), Vol.25(1), pp.1-6
2018
DOI: 10.5385/nm.2018.25.1.1
url
https://doi.org/10.5385/nm.2018.25.1.1View
Published (Version of record) Open Access

Abstract

Extremely low birth weight infants remain at increased risk of intraventricular hemorrhage from the fragile vascular bed of the germinal matrix; the roles of hypotension (ischemia) and reperfusion (hyperemia) in the development of intraventricular hemorrhage are still debated. Cerebrovascular pressure autoregulation protects the brain by maintaining constant cerebral blood flow despite changes in blood pressure. The ontogeny of cerebrovascular pressure autoregulation has not been well established and uncertainty remains about the optimal arterial blood pressure required to support brain perfusion. Another important aspect of premature cerebral hemodynamics is the critical closing pressure––the arterial blood pressure at which cerebral blood flow ceases. Interestingly, in premature infants, the critical closing pressure approximates the mean arterial blood pressure. Often in this unique population, cerebral blood flow occurs only during systole when the diastolic arterial blood pressure is equal to the critical closing pressure. Moreover, the diastolic closing margin, a metric of cerebral perfusion that normalizes diastolic arterial blood pressure to the critical closing pressure, may be a better measure than arterial blood pressure for defining cerebral perfusion in premature infants. Elevated diastolic closing margin has been associated with intraventricular hemorrhage. This review summarizes the current state of understanding of cerebral hemodynamics in premature infants.

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