POST-RESUSCITATION CEREBRAL PROTECTION

Ömer Emgin1
Adnan Ata2

1Kocaeli City Hospital, Department of Intensive Care, Kocaeli, Türkiye
2Kocaeli City Hospital, Department of Intensive Care, Kocaeli, Türkiye

Emgin Ö, Ata A. Post-Resuscitation Cerebral Protection. In: Turan S, editor. Hard Decisions in Intensive Care Unit. 1st ed. Ankara: Türkiye Klinikleri; 2025. p.161-176.

ABSTRACT

Return of Spontaneous Circulation (ROSC) following cardiac arrest is a critical stage for survival and neurological recovery. However, the post-ROSC process brings with it a complex pathophysiological manifestation defined as “Post-Cardiac Arrest Syndrome” (PCAS), which is characterized by hemodynamic imbalances, metabolic abnormalities, neurological damage, and systemic inflammatory responses. Brain damage is among the most common causes of mortality and morbidity in the post-ROSC period. In global ischemia during cardiac arrest, the cerebral circulation, which receives approximately 15-20% of the cardiac output, is significantly affected. As a result, cerebral hypoxia and reperfusion injury develop, which constitute one of the most common causes of mortality and morbidity in the post-ROSC period. Brain protection strategies aim to alleviate Post-Cardiac Arrest Brain Injury (PCABI) following ROSC and improve the long-term outcomes of patients. In our present day, international organizations (e.g., the American Heart Association (AHA) and the European Resuscitation Council (ERC) recommend Targeted Temperature Management (TTM) as a standard component of Post-Cardiac Arrest Care. TTM reduces oxygen consumption by slowing cerebral metabolism through therapeutic hypothermia and exerts a neuroprotective effect by limiting cerebral edema. This process mitigates brain injury through mechanisms such as the suppression of oxidative stress, inhibition of cellular apoptosis, reduction of neuroinflammation, and preservation of mitochondrial function. TTM is recommended to be applied at a target temperature of 32-36°C, particularly in comatose patients. However, debates continue regarding the optimal duration and target temperature of TTM. Additionally, the determination of neurological prognosis in post-cardiac arrest patients should be conducted meticulously through clinical and electrophysiological evaluations. Neuroimaging modalities, including magnetic resonance imaging and computed tomography, as well as neurophysiological assessment methods, such as electroencephalography and somatosensory evoked potentials, can be utilized to evaluate the patient’s potential for neurological recovery. In conclusion, the primary goal of neuroprotective treatment following ROSC is to manage the systemic effects of post-cardiac arrest syndrome and minimize neurological sequelae, thereby improving long-term survival. Current evidence suggests that individualized treatment approaches and multidisciplinary collaboration are among the most critical factors influencing post-ROSC prognosis. The integration of evidence-based therapeutic strategies into clinical practice is essential to achieving optimal outcomes in the management of post-ROSC patients.

Keywords: Post-cardiac arrest syndrome; Hypoxia, brain; Hypoxic brain damage; Targeted temperature management; Hypothermia, induced

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