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• W4207059340 abstract "We have read with great interest the letter to the editor written by Dr Griesdale and Dr Sekhon, responding positively to our recent article regarding the association between high SjvO2 values and unfavourable outcome.1.Richter J. Sklienka P. Chatterjee N. Maca J. Zahorec R. Burda M. Elevated jugular venous oxygen saturation after cardiac arrest.Resuscitation. 2021; 169: 214-219https://doi.org/10.1016/j.resuscitation.2021.10.011Google Scholar We agree entirely with the view that we need to focus on mechanisms responsible for cerebral hypoxia, observed following cardiac arrest, specifically the possible impaired oxygen diffusion due to cerebral oedema. Timely and sufficient delivery of oxygen to brain tissue is essential, and therefore the circulatory system has evolved through evolution to minimize the diffusion distance between supplying capillaries and neurons. Under physiological conditions, most neurons are within 20 μm of the nearest capillary.2.Wong A.D. Ye M. Levy A.F. et al.The blood-brain barrier: an engineering perspective.Front Neuroeng. 2013; 30: 7https://doi.org/10.3389/fneng.2013.00007Google Scholar Cerebral oedema following anoxic brain injury prolongs this distance because of two reasons; (i) the presence of oedema itself, and (ii) occlusion (at least partial) of brain capillaries by compressive effects of oedema. There is a risk of exceeding the critical diffusion distance, the maximum distance between the neuron and the O2 source, without causing anoxia and functional impairment.3.Boveris D.L. Boveris A. Oxygen delivery to the tissues and mitochondrial respiration.Front Biosci. 2007; 1: 1014-1023https://doi.org/10.2741/2121Google Scholar Despite long-standing recognition of cerebral oedema as a fundamental feature of brain injury following cardiac arrest and its potential for determining prognosis, it has not received the due attention it probably deserves. One possible explanation for this so far vague approach to cerebral oedema after cardiac arrest might be because it has only rarely been associated with the development of intracranial hypertension (defined as an intracranial pressure of more than 20 mm Hg). The Brain Trauma Foundation initially defined this threshold in 2007 for patients with severe traumatic brain injury (TBI) (level II recommendation).4.Brain Trauma Foundation American Association of Neurological Surgeons Congress of Neurological Surgeons Guidelines for the management of severe traumatic brain injury.J Neurotrauma. 2007; 24 (S1-106)https://doi.org/10.1089/neu.2007.9999Google Scholar It was also recommended to start intervention once the threshold is reached. Eventually, this recommendation was adopted for all brain injury patients. Intracranial pressure in patients after cardiac arrest rarely reached the threshold for intracranial hypertension.5.Deakin C.D. Nolan J.P. Soar J. et al.European Resuscitation Council Guidelines for Resuscitation 2010 Section 4. Adult advanced life support.Resuscitation. 2010; 81: 1305-1352https://doi.org/10.1016/j.resuscitation.2010.08.017Google Scholar Therefore, despite knowing cerebral oedema's existence, it was not considered an indication for therapeutic intervention. However, there is at least one significant difference between brain injury in patients after cardiac arrest and TBI. While both situations might lead to cytotoxic and vasogenic oedema, only severe TBI is frequently associated with at least one type of intracranial haemorrhage (e.g., epidural, subdural, subarachnoid, intraparenchymal haemorrhage or their combination), which can significantly affect the value of intracranial pressure. Therefore, it is possible that the recommended threshold for initiating therapeutic interventions in TBI patients is not appropriate for patients after cardiac arrest. Therefore, we believe that one of the ways we should focus on is searching for an effective therapeutic strategy to mitigate the development of cerebral oedema formation regardless of intracranial pressure values. The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper." @default.
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• W4207059340 date "2022-01-01" @default.
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• W4207059340 title "Reply to: “Correspondence to: Elevated jugular venous oxygen saturation after cardiac arrest”" @default.
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• W4207059340 doi "https://doi.org/10.1016/j.resuscitation.2021.12.019" @default.
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