Pathophysiology and the Monitoring Methods for Cardiac Arrest Associated Brain Injury

Abstract

Cardiac arrest (CA) is a well-known cause of global brain ischemia. After CA and subsequent loss of consciousness, oxygen tension starts to decline and leads to a series of cellular changes that will lead to cellular death, if not reversed immediately, with brain edema as a result. The electroencephalographic activity starts to change as well. Although increased intracranial pressure (ICP) is not a direct result of cardiac arrest, it can still occur due to hypoxic-ischemic encephalopathy induced changes in brain tissue, and is a measure of brain edema after CA and ischemic brain injury. In this review, we will discuss the pathophysiology of brain edema after CA, some available techniques, and methods to monitor brain oxygen, electroencephalography (EEG), ICP (intracranial pressure), and microdialysis on its measurement of cerebral metabolism and its usefulness both in clinical practice and possible basic science research in development. With this review, we hope to gain knowledge of the more personalized information about patient status and specifics of their brain injury, and thus facilitating the physicians’ decision making in terms of which treatments to pursue.

Targeted Temperature Management and Multimodality Monitoring of Comatose Patients After Cardiac Arrest

“…The eventual influx of sodium, chloride, and water into cells forms the basis of cytotoxic edema, which occurs during CA and other neurologic injuries. In addition, membrane depolarization results in the intracellular accumulation of calcium with activation of voltage gated calcium channels, as well as release of excitatory amino acid transmitters such as glutamate, perpetuating calcium and sodium influx into the neuron ( 5 , 8 ).…”

“…Accumulation of calcium ions in the mitochondria increases free radical production and mitochondrial permeability transition (MPT), resulting in mitochondrial swelling, oxidative damage, loss of ATP production, and cell death. Cellular accumulation of calcium in the cytosol additionally triggers lipolysis, membrane destabilization, proteolysis, nitric oxide production, and endonuclease DNA degradation ( 5 , 8 ). In vivo measurements of calcium demonstrate that in the acute ischemic period, cytosolic levels increase exponentially within 8 min of ischemia in vulnerable brain regions, although levels can return to baseline within 30–60 min if reperfusion occurs ( 5 , 10 ).…”

“…ICP monitoring is frequently used when cerebral edema is diagnosed in brain injured patients, including those with traumatic brain injury, intracerebral hemorrhage, or subarachnoid hemorrhage. Uncontrolled intracranial hypertension is associated with poor outcomes in the TBI literature, and although its impact in CA patients is not well defined, ICP elevations can result in cerebral herniation and may serve as a trigger for monitoring and augmenting cerebral perfusion pressures (CPP) ( 8 ).…”

Mean arterial pressure is associated with the neurological function in patients who survived after cardiopulmonary resuscitation: A retrospective cohort study

“…When cardiac arrest occurs, consciousness disorder may occur within 5 to 10 seconds, pupil dilation may occur within 30 to 60 seconds, and irreversible brain injury may occur after cardiac arrest exceeds 4 to 6 minutes. 15 Cerebral blood flow depends on cerebral perfusion pressure, which is equal to MAP minus intracranial pressure. Therefore, MAP is one of the essential factors affecting cerebral blood flow.…”

Pretreatment with human urine‑derived stem cells protects neurological function in rats following cardiopulmonary resuscitation after cardiac arrest

“…Cardiac arrest (CA) for >5 min often leads to irreversible brain damage ( 1 ). Implementing effective brain resuscitation to save ischemic neurons and accelerate the repair of damaged nerve tissue to maintain normal nerve function has become a global challenge ( 2 , 3 ), but the study of drug-induced cerebral resuscitation has progressed slowly ( 4 , 5 ).…”