Christian Crouzet , PhD 1 , 2 , 6 , Robert H. Wilson , PhD 1 , 6 , Donald Lee , BS 3 , 6 , Afsheen Bazrafkan , BS 3 , 6 , Bruce J. Tromberg , PhD 1 , 2 , 4 , 6 , Yama Akbari , MD, PhD , 1 , 3 , 6 , Bernard Choi , PhD , 1 , 2 , 4 , 5 , 6
04 January 2020
cardiac arrest, cerebral autoregulation, cerebral blood flow, electroencephalography, laser speckle imaging, perfusion, pulsatile, Imaging, Blood Pressure, Cardiopulmonary Arrest, Cardiopulmonary Resuscitation and Emergency Cardiac Care, Hemodynamics
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.
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.
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.