Cortical Anoxic Spreading Depolarization During Cardiac Arrest is Associated with Remote Effects on Peripheral Blood Pressure and Postresuscitation Neurological Outcome

• Published in: Neurocritical care Vol. 37; no. Suppl 1; pp. 139 - 154
• Main Authors: Han, Sangwoo, Contreras, Mayra Isabel, Bazrafkan, Afsheen, Rafi, Masih, Dara, Shirin M., Orujyan, Ani, Panossian, Anais, Crouzet, Christian, Lopour, Beth, Choi, Bernard, Wilson, Robert H., Akbari, Yama
• Format: Journal Article
• Language: English
• Published: New York Springer US 01-06-2022; Springer Nature B.V
• Subjects: Animals; Asphyxia - complications; Blood Pressure; Cardiac arrest; Cerebral Cortex; Cerebrovascular Circulation - physiology; Critical Care Medicine; Electrodes; Experiments; Heart Arrest - complications; Hemodynamics; Hypoxia; Intensive; Internal Medicine; Ischemia; Laboratories; Male; Medicine; Medicine & Public Health; Neurology; Neurosurgery; Rats; Rodents; Spreading Cortical Depolarization; Spreading Depolarizations; Traumatic brain injury; Ventilators; Cortical spreading depolarization; Anoxic spreading depolarization; Cardiac arrest; Spreading ischemia; Peripheral hemodynamics; Cerebral hemodynamics; Neurovascular coupling
• ISSN: 1541-6933; 1556-0961
• DOI: 10.1007/s12028-022-01530-2

Background
Spreading depolarizations (SDs) are self-propagating waves of neuronal and glial depolarizations often seen in neurological conditions in both humans and animal models. Because SD is thought to worsen neurological injury, the role of SD in a variety of cerebral insults has garnered significant investigation. Anoxic SD is a type of SD that occurs because of anoxia or asphyxia. Although asphyxia leading to a severe drop in blood pressure may affect cerebral hemodynamics and is widely known to cause anoxic SD, the effect of anoxic SD on peripheral blood pressure in the extremities has not been investigated. This relationship is especially important to understand for conditions such as circulatory shock and cardiac arrest that directly affect both peripheral and cerebral perfusion in addition to producing anoxic SD in the brain.
Methods
In this study, we used a rat model of asphyxial cardiac arrest to investigate the role of anoxic SD on cerebral hemodynamics and metabolism, peripheral blood pressure, and the relationship between these variables in 8- to 12-week-old male rats. We incorporated a multimodal monitoring platform measuring cortical direct current simultaneously with optical imaging.
Results
We found that during anoxic SD, there is decoupling of peripheral blood pressure from cerebral blood flow and metabolism. We also observed that anoxic SD may modify cerebrovascular resistance. Furthermore, shorter time difference between anoxic SDs measured at different locations in the same rat was associated with better neurological outcome on the basis of the recovery of electrocorticography activity (bursting) immediately post resuscitation and the neurological deficit scale score 24 h post resuscitation.
Conclusions
To our knowledge, this is the first study to quantify the relationship between peripheral blood pressure, cerebral hemodynamics and metabolism, and neurological outcome in anoxic SD. These results indicate that the characteristics of SD may not be limited to cerebral hemodynamics and metabolism but rather may also encompass changes in peripheral blood flow, possibly through a brain–heart connection, providing new insights into the role of anoxic SD in global ischemia and recovery.