Ontogeny of cerebrovascular critical closing pressure

Christopher J. Rhee*, Charles D. Fraser, Kathleen Kibler, Ronald B. Easley, Dean B. Andropoulos, Marek Czosnyka, Georgios V. Varsos, Peter Smielewski, Craig G. Rusin, Kenneth Martin Brady, Jeffrey R. Kaiser

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

8 Scopus citations

Abstract

Background: Premature infants are at risk of vascular neurologic insults. Hypotension and hypertension are considered injurious, but neither condition is defined with consensus. Cerebrovascular critical closing pressure (CrCP) is the arterial blood pressure (ABP) at which cerebral blood flow (CBF) ceases. CrCP may serve to define subject-specific low or high ABP. Our objective was to determine the ontogeny of CrCP.Methods:Premature infants (n = 179) with gestational age (GA) from 23-31 wk had recordings of ABP and middle cerebral artery flow velocity twice daily for 3 d and then daily for the duration of the first week of life. All infants received mechanical ventilation. CrCP was calculated using an impedance-model derivation with Doppler-based estimations of cerebrovascular resistance and compliance. The association between GA and CrCP was determined in a multivariate analysis.Results:The median (interquartile range) CrCP for the cohort was 22 mm Hg (19-25 mm Hg). CrCP increased significantly with GA (r = 0.6; slope = 1.4 mm Hg/wk gestation), an association that persisted with multivariate analysis (P < 0.0001).Conclusion:CrCP increased significantly from 23 to 31 wk gestation. The low CrCP observed in very premature infants may explain their ability to tolerate low ABP without global cerebral infarct or hemorrhage.

Original languageEnglish (US)
Pages (from-to)71-75
Number of pages5
JournalPediatric research
Volume78
Issue number1
DOIs
StatePublished - Jul 20 2015

ASJC Scopus subject areas

  • Pediatrics, Perinatology, and Child Health

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