Optimal oxygenation during and after cardiopulmonary resuscitation.
ABSTRACT Reversal of tissue hypoxia, particularly in the heart and brain, is a fundamental goal of cardiopulmonary resuscitation. However, a growing body of evidence suggests that hyperoxia, especially after return of spontaneous circulation (ROSC), may worsen outcomes. The purpose of this review is to describe the current evidence supporting the concept of controlled oxygenation during and after cardiac arrest.
Animal studies over the last two decades have built a compelling case that arterial hyperoxemia during the first hour after ROSC causes increased oxidative damage, increased neuronal death, and worse neurologic function. However, human data are limited. The only prospective randomized clinical trial comparing different inspired oxygen concentrations in post-cardiac arrest patients was underpowered to detect a difference in survival or neurologic outcome. More recently a retrospective analysis of data from a multicenter registry found that initial arterial hyperoxemia (paO2 ≥ 300 mmHg) was associated with increased mortality and worse functional outcome in patients admitted to the ICU after cardiac arrest. The existing evidence, though limited, has contributed to new guidelines for oxygen therapy in patients resuscitated from cardiac arrest.
The benefit of supplemental oxygen during cardiopulmonary resuscitation remains uncertain. However, in patients who achieve ROSC after cardiac arrest, available evidence supports adjusting inspired oxygen content to avoid arterial hyperoxemia while providing adequate arterial oxyhemoglobin saturation. This strategy is likely to be most effective when initiated as soon as possible after ROSC and appears to be most important during the first hour. Definitive clinical trials are needed to determine the ultimate impact on outcome.
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ABSTRACT: Oxygen is one of the most frequently-used therapeutic agents in medicine and the most commonly administered drug by prehospital personnel. There is increasing evidence of harm with too much supplemental oxygen in certain conditions, including stroke, chronic obstructive pulmonary disease (COPD), neonatal resuscitations, and in postresuscitation care. Recent guidelines published by the British Thoracic Society (BTS) advocate titrated oxygen therapy, but these guidelines have not been widely adapted in the out-of-hospital setting where high-flow oxygen is the standard. This report is a description of the implementation of a titrated oxygen protocol in a large urban-suburban Emergency Medical Services (EMS) system and a discussion of the practical application of this out-of-hospital protocol. Bosson N , Gausche-Hill M , Koenig W . Implementation of a titrated oxygen protocol in the out-of-hospital setting. Prehosp Disaster Med. 2014;28(4):1-6 .Prehospital and disaster medicine: the official journal of the National Association of EMS Physicians and the World Association for Emergency and Disaster Medicine in association with the Acute Care Foundation 07/2014; 29(04):1-6. DOI:10.1017/S1049023X14000570
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ABSTRACT: 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.Critical care (London, England) 10/2014; 18(5):555. DOI:10.1186/s13054-014-0555-4
Resuscitation 07/2014; 85(9). DOI:10.1016/j.resuscitation.2014.06.026 · 3.96 Impact Factor