The 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, Ken M. Brady, Jeffrey R. Kaiser

Research output: Contribution to journalArticlepeer-review

3 Scopus citations


Premature infants are at risk of vascular neurological insults. Hypotension and hypertension are considered injurious, but neither condition is defined with consensus. Critical closing pressure (CrCP) is the arterial blood pressure (ABP) at which cerebral blood flow ceases. CrCP may serve to define subject-specific low or high ABP. Our objective was to quantify CrCP as a function of gestational age (GA). One hundred eighty-six premature infants with a GA range of 23–33 weeks, were monitored with umbilical artery catheters and transcranial Doppler insonation of middle cerebral artery flow velocity (FV) for 1-h sessions over the first week of life. CrCP was calculated using an impedance model derivation with Doppler-based estimations of cerebrovascular resistance and compliance. CrCP increased significantly with GA (r = 0.47; slope = 1.4 mmHg/week gestation), an association that persisted with multivariate analysis (p < 0.001). Higher diastolic ABP and higher GA were associated with increased CrCP (p <0.001 for both). CrCP increases significantly at the end of the second and beginning of the third trimester. The low CrCP observed in premature infants may explain their ability to tolerate low ABP without global cerebral infarct or hemorrhage.

Original languageEnglish (US)
Pages (from-to)249-253
Number of pages5
JournalActa Neurochirurgica, Supplementum
StatePublished - May 1 2016

All Science Journal Classification (ASJC) codes

  • Surgery
  • Clinical Neurology


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