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J Am Heart Assoc. 2020 Jan 7;9(1):e012691. doi: 10.1161/JAHA.119.012691. Epub 2020 Jan 4.

Dissociation of Cerebral Blood Flow and Femoral Artery Blood Pressure Pulsatility After Cardiac Arrest and Resuscitation in a Rodent Model: Implications for Neurological Recovery.

Crouzet C1,2,3, Wilson RH1,3, Lee D4,3, Bazrafkan A4,3, Tromberg BJ1,2,5,3, Akbari Y1,4,3, Choi B1,2,5,6,3.

Author information

1
Beckman Laser Institute and Medical Clinic Irvine CA.
2
Department of Biomedical Engineering University of California Irvine CA.
3
University of California, Irvine Irvine CA.
4
Department of Neurology University of California Irvine CA.
5
Department of Surgery University of California Irvine CA.
6
Edwards Lifesciences Center for Advanced Cardiovascular Technology Irvine CA.

Abstract

Background Impaired neurological function affects 85% to 90% of cardiac arrest (CA) survivors. Pulsatile blood flow may play an important role in neurological recovery after CA. Cerebral blood flow (CBF) pulsatility immediately, during, and after CA and resuscitation has not been investigated. We characterized the effects of asphyxial CA on short-term (<2 hours after CA) CBF and femoral arterial blood pressure (ABP) pulsatility and studied their relationship to cerebrovascular resistance (CVR) and short-term neuroelectrical recovery. Methods and Results Male rats underwent asphyxial CA followed by cardiopulmonary resuscitation. A multimodal platform combining laser speckle imaging, ABP, and electroencephalography to monitor CBF, peripheral blood pressure, and brain electrophysiology, respectively, was used. CBF and ABP pulsatility and CVR were assessed during baseline, CA, and multiple time points after resuscitation. Neuroelectrical recovery, a surrogate for neurological outcome, was assessed using quantitative electroencephalography 90 minutes after resuscitation. We found that CBF pulsatility differs significantly from baseline at all experimental time points with sustained deficits during the 2 hours of postresuscitation monitoring, whereas ABP pulsatility was relatively unaffected. Alterations in CBF pulsatility were inversely correlated with changes in CVR, but ABP pulsatility had no association to CVR. Interestingly, despite small changes in ABP pulsatility, higher ABP pulsatility was associated with worse neuroelectrical recovery, whereas CBF pulsatility had no association. Conclusions Our results reveal, for the first time, that CBF pulsatility and CVR are significantly altered in the short-term postresuscitation period after CA. Nevertheless, higher ABP pulsatility appears to be inversely associated with neuroelectrical recovery, possibly caused by impaired cerebral autoregulation and/or more severe global cerebral ischemia.

KEYWORDS:

cardiac arrest; cerebral autoregulation; cerebral blood flow; electroencephalography; laser speckle imaging; perfusion; pulsatile

PMID:
31902319
DOI:
10.1161/JAHA.119.012691
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