How much oxygen in adult cardiac arrest?

Dell’Anna, Antonio Maria; Lamanna, Irene; Vincent, Jean‐Louis; Taccone, Fabicpro Silvio

doi:10.1186/s13054-014-0555-4

Cited by 32 publications

(32 citation statements)

References 39 publications

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“…Upon ROSC, reperfusion injury occurs as a result of oxygen free radical production, which leads to intracellular oxidation [62]. Examples include superoxide (O 2 − ), hydrogen peroxide (H 2 O 2 ), hydroxyl anion (OH − ), and nitrite (NO 2 − ).…”

Section: Secondary Injurymentioning

confidence: 99%

Clinical pathophysiology of hypoxic ischemic brain injury after cardiac arrest: a “two-hit” model

2017

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Hypoxic ischemic brain injury (HIBI) after cardiac arrest (CA) is a leading cause of mortality and long-term neurologic disability in survivors. The pathophysiology of HIBI encompasses a heterogeneous cascade that culminates in secondary brain injury and neuronal cell death. This begins with primary injury to the brain caused by the immediate cessation of cerebral blood flow following CA. Thereafter, the secondary injury of HIBI takes place in the hours and days following the initial CA and reperfusion. Among factors that may be implicated in this secondary injury include reperfusion injury, microcirculatory dysfunction, impaired cerebral autoregulation, hypoxemia, hyperoxia, hyperthermia, fluctuations in arterial carbon dioxide, and concomitant anemia.Clarifying the underlying pathophysiology of HIBI is imperative and has been the focus of considerable research to identify therapeutic targets. Most notably, targeted temperature management has been studied rigorously in preventing secondary injury after HIBI and is associated with improved outcome compared with hyperthermia. Recent advances point to important roles of anemia, carbon dioxide perturbations, hypoxemia, hyperoxia, and cerebral edema as contributing to secondary injury after HIBI and adverse outcomes. Furthermore, breakthroughs in the individualization of perfusion targets for patients with HIBI using cerebral autoregulation monitoring represent an attractive area of future work with therapeutic implications.We provide an in-depth review of the pathophysiology of HIBI to critically evaluate current approaches for the early treatment of HIBI secondary to CA. Potential therapeutic targets and future research directions are summarized.

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Section: Secondary Injurymentioning

confidence: 99%

Clinical pathophysiology of hypoxic ischemic brain injury after cardiac arrest: a “two-hit” model

2017

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“…While the grafts and recipients were very heterogeneous in the study by Watson et al ., the same deleterious effect of high PaO2 has already been shown by others, where hyperoxia caused severe hepatic reperfusion injury . The negative effect of high oxygen contents during NMP is also supported by evidence during CPB or during resuscitation after cardiac arrest . Of note, most of human and porcine studies provided arterialized blood through the PV, while only few provided partially oxygenated blood .…”

Section: Discussionmentioning

confidence: 79%

Perfusion settings and additives in liver normothermic machine perfusion with red blood cells as oxygen carrier. A systematic review of human and porcine perfusion protocols

et al. 2018

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Liver machine perfusion (MP) at normothermic temperature (NMP) is a promising way to preserve and evaluate extended criteria donor livers. Currently, no consensus exists in methodology and perfusion protocols. Here, the authors performed a systematic literature search to identify human and porcine studies reporting on liver NMP with red blood cells. A qualitative synthesis was performed concerning technical aspects of MP, fluid composition, gas supply, and liver positioning. Thirty-seven publications including 11 human and 26 porcine studies were considered for qualitative synthesis. Control mode, pressure, flow, perfusate additives, and targeted blood gas parameters varied across human as well as porcine studies. For future analyses, it is advisable to report flow adjusted to liver weight and exact pressure parameters including mean, systolic, and diastolic pressure. Parenteral nutrition and insulin addition was common. Parenteral nutrition included amino acids and/or glucose without lipids. Taurocholic acid derivatives were used as bile flow promoters. However, short-term human NMP without taurocholic acid derivatives seems to be possible. This finding is relevant due to the lack of clinical grade bile salts. Near physiological oxygen tension in the perfusate is doable by adjusting gas flows, while blood gas parameters regulation needs more detailed description.

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“…The high concentration of oxygen can stimulate ROS production, worsen cellular and mitochondrial function. Furthermore, hyperoxemia causes vasoconstriction and induces myocardial ischemia being deleterious for brain perfusion as well as promoting seizures [13].…”

Section: Pre-hospital Oxygenation After Roscmentioning

confidence: 99%