Optimal oxygenation during and after cardiopulmonary resuscitation
Center for Resuscitation Science and Department of Emergency Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA. Current opinion in critical care
(Impact Factor: 2.62).
03/2011; 17(3):236-40. DOI: 10.1097/MCC.0b013e3283454c8c
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.
Available from: Elzbieta Salinska
- "There is a lot of recent evidence that hyperbaric oxygen (HBO) prevents neuronal damage and improves neurological outcome after cardiac arrest or stroke (for review see Harch and Neubauer 2009), and there is the opinion that amount of oxygen delivered to the brain in a short time after cardiac arrest or after stroke may be an important factor in preventing neuronal damage resulted from brain ischemia (Neumar 2011; Rosenthal et al. 2003; Van Meter et al. 2008). The neurological outcome after cardiac arrest may be greatly affected by the oxygen inhaled immediately after resuscitation, and there is a growing body of evidence suggesting that delivering too much oxygen too quickly may increase injury associated with postischemic reperfusion. "
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ABSTRACT: Anoxic brain injury resulting from cardiac arrest is responsible for approximately two-thirds of deaths. Recent evidence suggests that increased oxygen delivered to the brain after cardiac arrest may be an important factor in preventing neuronal damage, resulting in an interest in hyperbaric oxygen (HBO) therapy. Interestingly, increased oxygen supply may be also reached by application of normobaric oxygen (NBO) or hyperbaric air (HBA). However, previous research also showed that the beneficial effect of hyperbaric treatment may not directly result from increased oxygen supply, leading to the conclusion that the mechanism of hyperbaric prevention of brain damage is not well understood. The aim of our study was to compare the effects of HBO, HBA and NBO treatment on gerbil brain condition after transient forebrain ischemia, serving as a model of cardiac arrest. Thereby, we investigated the effects of repetitive HBO, HBA and NBO treatment on hippocampal CA1 neuronal survival, brain temperature and gerbils behavior (the nest building), depending on the time of initiation of the therapy (1, 3 and 6 h after ischemia). HBO and HBA applied 1, 3 and 6 h after ischemia significantly increased neuronal survival and behavioral performance and abolished the ischemia-evoked brain temperature increase. NBO treatment was most effective when applied 1 h after ischemia; later application had a weak or no protective effect. The results show that HBO and HBA applied between 1 and 6 h after ischemia prevent ischemia-evoked neuronal damage, which may be due to the inhibition of brain temperature increase, as a result of the applied rise in ambient pressure, and just not due to the oxygen per se. This perspective is supported by the finding that NBO treatment was less effective than HBO or HBA therapy. The results presented in this paper may pave the way for future experimental studies dealing with pressure and temperature regulation.
Available from: Fabrizio Proietti
- "Measurements of lipid peroxidation to quantitate oxidative damage are becoming more commonly used to implicate free radicals in pathophysiology. There has been an increased focus on the possible negative effects of arterial hyperoxia that can occur as a result of the use of supplementary oxygen in resuscitating both neonates and adults   . The implications of the effects of oxidative damage and lipid peroxidation are highly relevant for asphyxiated newborns, for patients with brain trauma or myocardial infarction, and for individuals suffering from numerous neurodegenerative diseases throughout their life span  . "
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ABSTRACT: Isoprostanes, neuroprostanes, isofurans, and neurofurans have all become attractive biomarkers of oxidative damage and lipid peroxidation in brain tissue. Asphyxia and subsequent reoxygenation cause a burst of oxygen free radicals. Isoprostanes and isofurans are generated by free radical attacks of esterified arachidonic acid. Neuroprostanes and neurofurans are derived from the peroxidation of docosahexanoic acid, which is abundant in neurons and could therefore more selectively represent oxidative brain injury. Newborn piglets (age 12-36 h) underwent hypoxia until the base excess reached -20 mmol/L or the mean arterial blood pressure dropped below 15 mm Hg. They were randomly assigned to receive resuscitation with 21, 40, or 100% oxygen for 30 min and then ventilation with air. The levels of isoprostanes, isofurans, neuroprostanes, and neurofurans were determined in brain tissue (ng/g) isolated from the prefrontal cortex using gas chromatography-mass spectrometry (GC/MS) with negative ion chemical ionization (NICI) techniques. A control group underwent the same procedures and observations but was not submitted to hypoxia or hyperoxia. Hypoxia and reoxygenation significantly increased the levels of isoprostanes, isofurans, neuroprostanes, and neurofurans in the cerebral cortex. Nine hours after resuscitation with 100% oxygen for 30 min, there was nearly a 4-fold increase in the levels of isoprostanes and isofurans compared to the control group (P=0.007 and P=0.001) and more than a 2-fold increase in neuroprostane levels (P=0.002). The levels of neuroprostanes and neurofurans were significantly higher in the piglets that were resuscitated with supplementary oxygen (40 and 100%) compared to the group treated with air (21%). The significance levels of the observed differences in neuroprostanes for the 21% vs 40% comparison and the 21% vs 100% comparison were P<0.001 and P=0.001, respectively. For neurofurans, the P values of the 21% vs 40% comparison and the 21% vs 100% comparison were P=0.036 and P=0.025, respectively. Supplementary oxygen used for the resuscitation of newborns increases lipid peroxidation in brain cortical neurons, a result that is indicative of oxidative brain damage. These novel findings provide new knowledge regarding the relationships between oxidative brain injury and resuscitation with oxygen.
Available from: Tomas Kovarnik
- "As shown in Additional file 3 and Table 2, both FF and FS ECMO regimens offered adequate (that is, not unintentionally high) brain and peripheral oxygenations expressed by regional O2 saturations immediatelly after ECMO initiation. Re-oxygenation on ECMO can be easily controlled when using on-line monitoring of blood gases as in our protocol, thus avoiding the possible adverse effects of arterial hyperoxemia on outcome after reperfusion/ROSC [46,47]. "
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Extracorporeal membrane oxygenation (ECMO) is increasingly used in cardiac arrest (CA). Adequacy of carotid and coronary blood flows (CaBF, CoBF) and coronary perfusion pressure (CoPP) in ECMO treated CA is not well established. This study compares femoro-femoral (FF) to femoro-subclavian (FS) ECMO and intraaortic balloon counterpulsation (IABP) contribution based on CaBF, CoBF, CoPP, myocardial and brain oxygenation in experimental CA managed by ECMO.
In 11 female pigs (50.3 ± 3.4 kg), CA was randomly treated by FF versus FS ECMO ± IABP. Animals under general anesthesia had undergone 15 minutes of ventricular fibrillation (VF) with ECMO flow of 5 to 10 mL/kg/min simulating low-flow CA followed by continued VF with ECMO flow of 100 mL/kg/min. CaBF and CoBF were measured by a Doppler flow wire, cerebral and peripheral oxygenation by near infrared spectroscopy. CoPP, myocardial oxygen metabolism and resuscitability were determined.
CaBF reached values > 80% of baseline in all regimens. CoBF > 80% was reached only by the FF ECMO, 90.0% (66.1, 98.6). Addition of IABP to FF ECMO decreased CoBF to 60.7% (55.1, 86.2) of baseline, P = 0.004. FS ECMO produced 70.0% (49.1, 113.2) of baseline CoBF, significantly lower than FF, P = 0.039. Addition of IABP to FS did not change the CoBF; however, it provided significantly higher flow, 76.7% (71.9, 111.2) of baseline, compared to FF + IABP, P = 0.026. Both brain and peripheral regional oxygen saturations decreased after induction of CA to 23% (15.0, 32.3) and 34% (23.5, 34.0), respectively, and normalized after ECMO institution. For brain saturations, all regimens reached values exceeding 80% of baseline, none of the comparisons between respective treatment approaches differed significantly. After a decline to 15 mmHg (9.5, 20.8) during CA, CoPP gradually rose with time to 68 mmHg (43.3, 84.0), P = 0 .003, with best recovery on FF ECMO. Resuscitability of the animals was high, both 5 and 60 minutes return of spontaneous circulation occured in eight animals (73%).
In a pig model of CA, both FF and FS ECMO assure adequate brain perfusion and oxygenation. FF ECMO offers better CoBF than FS ECMO. Addition of IABP to FF ECMO worsens CoBF. FF ECMO, more than FS ECMO, increases CoPP over time.
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