TL;DR: It is shown that asphyxia of newborn infants causes oxidative stress, and that resuscitating them with 100% oxygen causes hyperoxemia and increases oxidative stress; and that room air might be preferable for resuscitating these infants.
Abstract: Although room air is adequate for resuscitating asphyxiated newborn infants, guidelines recommend using 100% oxygen. Hyperoxemia, as has been noted in animal studies, could cause delayed breathing, increased oxygen consumption, and disordered cerebral circulation. In addition, 100% oxygen has caused prolonged oxidation of blood glutathione in neonates. In this study, 51 asphyxiated neonates born at term were randomly assigned to resuscitation with room air (RAR) and 55 to resuscitation with 100% oxygen (OxR). The goal was to learn whether using oxygen for resuscitation triggers oxidative stress. Critical criteria were the Apgar score, the time of the first cry, and sustained respiration. Signs of asphyxia included hypotonia, apnea, a lack of response to external stimuli, pallor, bradycardia, and acidosis. Cesarean delivery was more than twice as frequent in asphyxiated infants than in control subjects, and 1- and 5-minute Apgar scores were reduced. Infants in both experimental groups took significantly longer to the first cry, but the RAR group needed less time of ventilation for resuscitation time than the OxR group (5.3 vs. 6.8 minutes). Hyperoxemia was associated with oxygen resuscitation but not with the use of room air (PO 2 of 126 and 72 mm Hg, respectively). Whole blood levels of reduced glutathione were decreased in both asphyxiated groups; and oxidized glutathione, glutathione cycle enzymes, and superoxide dismutase activity were increased. These changes were, however, significantly greater in the OxR group than in RAR infants. Follow up after the first week of lite and at age 4 weeks showed no differences between the experimental groups. These findings show that asphyxia of newborn infants causes oxidative stress, and that resuscitating them with 100% oxygen causes hyperoxemia and increases oxidative stress. The investigators conclude that room air might be preferable for resuscitating these infants.
TL;DR: It is concluded that both hypoxemia and extreme hyperoxemia are associated with increased mortality and a decrease in good outcomes among TBI patients.
Abstract: An association between hypoxemia and poor outcomes from traumatic brain injury (TBI) is well documented. However, it is unclear whether hyperoxygenation is beneficial. This registry-based analysis explores the relationship between early hypoxemia and hyperoxemia on outcome from moderate-to-severe TBI. TBI patients (Abbreviated Injury Scale score 3+) were identified from the San Diego County trauma registry. Patients were stratified by arrival partial oxygen pressure (Po2) value. Trauma and injury severity score (TRISS) was then used to calculate predicted survival for each patient, with the mean observed-predicted survival differential determined for each arrival Po2 stratification. Logistic regression was used to quantify the relationship between hypoxemia, hyperoxemia, and outcome from TBI after adjusting for multiple variables including intubation and ventilation status. A total of 3420 patients were included in the analysis. TRISS calculations revealed worse outcomes than predicted for both h...
TL;DR: Eubarichyperoxemia improves neurological and neuropathological outcome, continuous oxygen therapy offers the greatest benefit, and reperfusion hyperoxemia is beneficial, and the findings should allay clinical concerns regarding oxygen‐induced reperfusions injury, and encourage clinical trials studying arterial hyperoxygenation in treating stroke.
Abstract: We explore three questions concerning arterial hyperoxygenation and focal ischemia. (1) Does greater benefit accrue with higher levels of arterial hyperoxemia? (2) Is the net effect of continuous (intraischemic plus postischemic) oxygen therapy toxic, or beneficial to middle cerebral artery infarction? (3) In view of free radical theories of reperfusion injury, does hyperoxia isolated to the reperfusion period damage tissue? Rats subjected to transient, focal, normothermic, normoglycemic ischemia were assessed at 2 weeks' survival. Arterial hyperoxygenation from 98.9 ± 4.0 to 312.2 ± 48.4mm Hg during ischemia improved (p < 0.05) neurological function, as did isolated reperfusion hyperoxemia, but treatment with continuous hyperoxemia both during and after ischemia yielded greatest benefit (p < 0.001). Cortical infarcts constituted 6.5 ± 1.8% of the hemisphere at normoxia, but 2.3 ± 0.9% at hyperoxic levels (p < 0.01). Hyperoxia isolated to the reperfusion period also reduced cortical necrosis, from 6.5% to 2.7 ± 1.2%. However, continuous intraischemic and reperfusion hyperoxemia led to only 0.2 ± 0.1% cortical necrosis (p = 0.0005). Increasing the degree of hyperoxemia did not augment the benefit. We conclude that (1) eubaric hyperoxemia improves neurological and neuropathological outcome, (2) continuous oxygen therapy offers the greatest benefit, and (3) reperfusion hyperoxemia is beneficial. The findings should allay clinical concerns regarding oxygen-induced reperfusion injury, and, by obviating hyperbaric chambers, encourage clinical trials studying arterial hyperoxemia in treating stroke.
TL;DR: In this article, a system and method for delivering fractionally inspired oxygen to a patient in response to receiving an arterial hemoglobin oxygen saturation signal (SpO2) are disclosed.
Abstract: A system and method for delivering fractionally inspired oxygen (FiO2) to a patient in response to receiving an arterial hemoglobin oxygen saturation signal (SpO2) are disclosed. The SpO2 is measured, for example, by using a pulse oximeter. An algorithm receives a signal indicating the SpO2. The algorithm determines wither the SpO2 is in the normoxemia range, hypoxemia range or hyperoxemia range. The algorithm also determines trends by calculating a slope of second-to-second changes in the SpO2. Based on the current SpO2 and the trend, the algorithm determines the appropriate FiO2 for the patient and instructs a device, such as a mechanical ventilator or an air oxygen mixer as to the appropriate FiO2 to be delivered to the patient. The system initializes various parameters with default values, but a user (e.g., a nurse) can also update the settings at any time. The system also provides alerts for various conditions, for example, standard pulse oximeter alarms, as well as notification when an episode of hyperoxemia or hypoxemia occurs, when it lasts for more than a specified period of time (e.g., two minutes) in spite of FiO2 adjustments and when the adjustments set the FiO2 at certain levels. The user is also alerted when SpO2 signal is lost.
TL;DR: It is hypothesized that hyperoxemia may be 1 of the triggering factors responsible for an increased oxidation of GSH (reduced glutathione), and an increased antioxidant enzyme activity, which reflects an oxidative stress, indicates that the antioxidant capacity of the newly born infant may have been surpassed.