How much oxygen in adult cardiac arrest?

Critical Care, Oct 2014

Although experimental studies have suggested that a high arterial oxygen pressure (PaO2) might aggravate post-anoxic brain injury, clinical studies in patients resuscitated from cardiac arrest (CA) have given conflicting results. Some studies found that a PaO2 of more than 300�mm Hg (hyperoxemia) was an independent predictor of poor outcome, but others reported no association between blood oxygenation and neurological recovery in this setting. In this article, we review the potential mechanisms of oxygen toxicity after CA, animal data available in this field, and key human studies dealing with the impact of oxygen management in CA patients, highlighting some potential confounders and limitations and indicating future areas of research in this field. From the currently available literature, high oxygen concentrations during cardiopulmonary resuscitation seem preferable, whereas hyperoxemia should be avoided in the post-CA care. A specific threshold for oxygen toxicity has not yet been identified. The mechanisms of oxygen toxicity after CA, such as seizure development, reactive oxygen species production, and the development of organ dysfunction, need to be further evaluated in prospective studies.

A PDF file should load here. If you do not see its contents the file may be temporarily unavailable at the journal website or you do not have a PDF plug-in installed and enabled in your browser.

Alternatively, you can download the file locally and open with any standalone PDF reader:

http://ccforum.com/content/pdf/s13054-014-0555-4.pdf

How much oxygen in adult cardiac arrest?

Critical Care How much oxygen in adult cardiac arrest? Antonio Maria Dell'Anna 0 Irene Lamanna 0 Jean-Louis Vincent 0 Fabio Silvio Taccone 0 0 Department of Intensive Care, Erasme Hospital, Université Libre de Bruxelles , Belgium, Route de Lennik 808, 1070 Brussels , Belgium Although experimental studies have suggested that a high arterial oxygen pressure (PaO2) might aggravate post-anoxic brain injury, clinical studies in patients resuscitated from cardiac arrest (CA) have given conflicting results. Some studies found that a PaO2 of more than 300 mm Hg (hyperoxemia) was an independent predictor of poor outcome, but others reported no association between blood oxygenation and neurological recovery in this setting. In this article, we review the potential mechanisms of oxygen toxicity after CA, animal data available in this field, and key human studies dealing with the impact of oxygen management in CA patients, highlighting some potential confounders and limitations and indicating future areas of research in this field. From the currently available literature, high oxygen concentrations during cardiopulmonary resuscitation seem preferable, whereas hyperoxemia should be avoided in the post-CA care. A specific threshold for oxygen toxicity has not yet been identified. The mechanisms of oxygen toxicity after CA, such as seizure development, reactive oxygen species production, and the development of organ dysfunction, need to be further evaluated in prospective studies. Introduction Sudden cardiac arrest (CA) is the leading cause of death among adults worldwide [ 1,2 ]. In most patients, attempts at cardiopulmonary resuscitation (CPR) remain ineffective and spontaneous cardiac activity cannot be restored [3]. Among those patients who do achieve return of spontaneous circulation (ROSC), there are two key periods when death may occur: early (during the first three days), usually because of recurrent CA or severe cardiovascular failure resulting in multiple organ failure (MOF), and late (beyond day 3), usually secondary to withdrawal of life-sustaining therapies in the absence of neurological recovery [ 4 ]. Although several interventions, including target temperature management (TTM), have been introduced into the postCA care of these patients [ 5,6 ], conflicting results have been obtained [7], and these approaches are not sufficient to prevent the deleterious consequences of brain ischemia in all patients. During the post-CA care, secondary brain insult must be avoided [ 8 ] and optimization of brain oxygenation is likely to be an important component of brain recovery. The restoration of adequate systemic hemodynamics is a prerequisite to provide adequate cerebral blood flow in CA patients [ 9,10 ], but brain oxygenation is also determined by the arterial oxygen content. Arterial oxygen pressure (PaO2) itself may influence brain cellular oxygen supply; if hypoxemia (that is, PaO2 of less than 60 mm Hg) is associated with poor outcomes after CA [11], a high PaO2 may also be detrimental in a vulnerable brain, as suggested in patients with traumatic brain injury or stroke [ 12,13 ]. The aims of this article are to review the potential mechanisms of oxygen toxicity after CA and to discuss the clinical impact of oxygen management on post-CA care. Post-cardiac arrest syndrome: the role of oxygen Post-cardiac arrest syndrome (PCAS) is a complex phenomenon, which shares several features with septic shock [ 7,14 ]. In particular, PCAS includes a systemic inflammatory response that can be triggered by the ischemia-reperfusion injury and also specific precipitating events, such as concomitant infections or heart disease. Moreover, PCAS can contribute to brain injury and myocardial dysfunction and can rapidly lead to MOF. The primary ischemia-reperfusion injury [15] activates various intracellular pathways, promoting ion concentration disequilibrium with increased intracellular levels of inorganic phosphate, lactate, and H+, and resulting in an influx of calcium into the cell [ 16 ], which aggravates mitochondrial dysfunction and eventually leads to programmed cellular death (apoptosis). After reperfusion has occurred, other mediators, including superoxide (O2−), peroxynitrite (NO2−), hydrogen peroxide (H2O2), and hydroxyl radicals (OH−), contribute to worsen cellular function by oxidizing and damaging numerous cellular components [ 17 ] (Figure 1). These reactive oxygen species (ROS) then have a central role in initiating and enhancing the post-ischemic damage [ 15 ]. Indeed, supra-normal oxygen concentrations in this context may further stimulate ROS production and contribute to worsen cellular function in a setting of impaired mitochondrial function and impaired oxygen utilization. Moreover, some other systemic detrimental effects of hyperoxemia have been known for many years [ 18-20 ]. Hyperoxemia causes systemic and coronary vasoconstriction, which can decrease cardiac output and induce m (...truncated)


This is a preview of a remote PDF: http://ccforum.com/content/pdf/s13054-014-0555-4.pdf

Antonio Dell�Anna, Irene Lamanna, Jean-Louis Vincent, Fabio Taccone. How much oxygen in adult cardiac arrest?, Critical Care, 2014, pp. 555, 18, DOI: 10.1186/s13054-014-0555-4