Brain injury in extracorporeal cardiopulmonary resuscitation: translational to clinical research

Abstract

The addition of extracorporeal membrane oxygenation (ECMO) to conventional cardiopulmonary resuscitation (CPR), termed extracorporeal cardiopulmonary resuscitation (ECPR), has significantly improved survival in selected patient populations. Despite this advancement, significant neurological impairment persists in approximately half of survivors. ECPR represents a potential advancement for patients who experience refractory cardiac arrest (CA) due to a reversible etiology and do not regain spontaneous circulation. Important risk factors for acute brain injury (ABI) in ECPR include lack of perfusion, reperfusion, and altered cerebral autoregulation. The initial hypoxic-ischemic injury caused by no-flow and low-flow states after CA and during CPR is compounded by reperfusion, hyperoxia during ECMO support, and nonpulsatile blood flow. Additionally, ECPR patients are at risk for Harlequin syndrome with peripheral cannulation, which can lead to preferential perfusion of cerebral vessels with deoxygenated blood. Lastly, the oxygenator membrane is prothrombotic and requires systemic anticoagulation. The two competing phenomena result in thrombus formation, hemolysis, and thrombocytopenia, increasing the risk of ischemic and hemorrhagic ABI. In addition to clinical studies, we assessed available ECPR animal models to identify the mechanisms underlying ABI at the cellular level. Standardized multimodal neurological monitoring may facilitate early detection of and intervention for ABI. With the increasing use of ECPR, it is critical to understand the pathophysiology of ABI, its prevention, and the management strategies for improving the outcomes of ECPR. Translational and clinical research focusing on acute ABI immediately after ECMO cannulation and its short-and long-term neurological outcomes are warranted.

Predicting Acute Brain Injury in Venoarterial Extracorporeal Membrane Oxygenation Patients with Tree-Based Machine Learning: Analysis of the Extracorporeal Life Support Organization Registry

“…Although cross-sectionally the ECMO pump ow rates were small and may not be clinically meaningful, over the duration of ECMO support these differences may accrue to substantial differences. While pre-ECMO cardiac arrest is a known risk factor for CNS ischemia in ECPR patients, (2,31) likely related to reperfusion injury and associated reactive oxygen species formation, (31,32) we also note that this factor was highly important in VV-ECMO patients (33) which has not been previously reported. These comparisons suggest there are similar underlying but overall divergent risk factors between these populations, which necessitates further investigation with prospective observational studies.…”

The state of emergency department extracorporeal cardiopulmonary resuscitation: Where are we now, and where are we going?

“…This intricate procedure demands procedural expertise, teamwork, and meticulous monitoring to ensure optimal blood flow and prevent complications. ECPR is integrated within a continuum of care, encompassing postresuscitation management, cardiac catheterization to address underlying causes, targeted temperature management to mitigate brain injury, 55 and ongoing monitoring of cardiac function 56 and neurological status 57,58 . The collaborative efforts of healthcare professionals from various disciplines are fundamental to this system, allowing for swift and strategic decision‐making throughout each stage of care, ultimately increasing the potential for improved patient outcomes.…”

Impact of Pulse Pressure on Acute Brain Injury in Venoarterial ECMO Patients with Cardiogenic Shock During the First 24 Hours of ECMO Cannulation: Analysis of the Extracorporeal Life Support Organization Registry

“…Induced by ECMO circuit, the absence of pulsatility is associated with reduced O 2 consumption and impaired cerebral autoregulation, potentially contributing to CNS ischemia. 21 Furthermore, low PP can indicate inadequate cardiac contractility, and thus systemic hypoperfusion, which may increase the risk of CNS ischemia. Interestingly, in contrast to previous literature describing that a larger delta PaCO 2 was associated with ICH, 42 our study demonstrated that delta PaCO 2 was associated with CNS ischemia rather than ICH.…”