Cessation of diastolic cerebral blood flow velocity: The role of critical closing pressure

Georgios V. Varsos*, Hugh K. Richards, Magdalena Kasprowicz, Matthias Reinhard, Peter Smielewski, Kenneth Martin Brady, John D. Pickard, Marek Czosnyka

*Corresponding author for this work

Research output: Contribution to journalArticle

17 Scopus citations

Abstract

Background: Reducing cerebral perfusion pressure (CPP) below the lower limit of autoregulation (LLA) causes cerebral blood flow (CBF) to become pressure passive. Further reductions in CPP can cause cessation of CBF during diastole. We hypothesized that zero diastolic flow velocity (FV) occurs when diastolic blood pressure becomes less than the critical closing pressure (CrCP). Methods: We retrospectively analyzed studies of 34 rabbits with CPP below the LLA, induced with pharmacologic sympathectomy (N = 23) or cerebrospinal fluid infusion (N = 11). Basilar artery blood FV and cortical Laser Doppler Flow (LDF) were monitored. CrCP was trended using a model of cerebrovascular impedance. The diastolic closing margin (DCM) was monitored as the difference between diastolic blood pressure and CrCP. LDF was recorded for DCM values greater than and less than zero. Results: Arterial hypotension caused a reduction of CrCP (p < 0.001), consistent with decreased wall tension (p < 0.001) and a drop in intracranial pressure (ICP; p = 0.004). Cerebrospinal infusion caused an increase of CrCP (p = 0.002) accounted for by increasing ICP (p < 0.001). The DCM was compromised by either arterial hypotension or intracranial hypertension (p < 0.001 for both). When the DCM reached zero, diastolic FV ceased for a short period during each heart cycle (R = 0.426, p < 0.001). CBF pressure passivity accelerated when DCM decreased below zero (from 1.51 ± 0.51 to 2.17 ± 1.17 % ΔLDF/ΔmmHg; mean ± SD; p = 0.010). Conclusions: The disappearance of diastolic CBF below LLA can be explained by DCM reaching zero or negative values. Below this point the decrease in CBF accelerates with further decrements of CPP.

Original languageEnglish (US)
Pages (from-to)40-48
Number of pages9
JournalNeurocritical Care
Volume20
Issue number1
DOIs
StatePublished - Feb 2014

Keywords

  • Brain ischemia
  • Cerebral autoregulation
  • Critical closing pressure
  • Vanishing diastolic flow velocity
  • Wall tension

ASJC Scopus subject areas

  • Clinical Neurology
  • Critical Care and Intensive Care Medicine

Fingerprint Dive into the research topics of 'Cessation of diastolic cerebral blood flow velocity: The role of critical closing pressure'. Together they form a unique fingerprint.

  • Cite this

    Varsos, G. V., Richards, H. K., Kasprowicz, M., Reinhard, M., Smielewski, P., Brady, K. M., Pickard, J. D., & Czosnyka, M. (2014). Cessation of diastolic cerebral blood flow velocity: The role of critical closing pressure. Neurocritical Care, 20(1), 40-48. https://doi.org/10.1007/s12028-013-9913-3