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Amniotic Fluid Embolism
Published in Vincenzo Berghella, Maternal-Fetal Evidence Based Guidelines, 2022
Zaid Diken, Antonio F. Saad, Luis D. Pacheco
Post cardiac arrest management is of paramount importance [40]. After ROSC, patients are often hemodynamic unstable, and management is mainly based on administration of fluids, vasopressors, and inotropes. Mean arterial blood pressure of 65–70 mmHg should be maintained [40]. To decrease ischemia-reperfusion injury, fever should be avoided and aggressively treated. Hyperoxia should be avoided for the same reason and administration of 100% oxygen to patients after survival of cardiac arrest is not recommended. This is achieved by weaning the inspired fraction of oxygen to sustain pulse oximetry values of 94–98% [41]. As standard of care in any critically ill patient, serum glucose levels should be maintained between 140 and 180 mg/dL with implementation of an insulin drip if needed.
Patient Transfer
Published in Ian Greaves, Keith Porter, Jeff Garner, Trauma Care Manual, 2021
Ian Greaves, Keith Porter, Jeff Garner
There is increasing evidence of the harm of over ventilation and oxygenation (hyperoxia). Evidence from the management of acute respiratory distress syndrome (ARDS) has clearly demonstrated the benefits of low tidal volume (Vt) (<6 mL/kg) based on ideal body weight and peak pressures below 30 cmH2O.21 It is worth noting that ideal body weight starts to plateau in males at around 100 kg and in females at 70 kg depending on which calculation is used.22 There is also evidence of benefit of lung-protective ventilation in other cohorts: a recent meta-analysis of intraoperative patients found a reduction in post-operative pneumonia if a low Vt (<8 mL/kg) and moderate to high PEEP > or equal to 5 cmH2O were used.23
Bronchoalveolar Lavage in Inhalation Lung Toxicity
Published in Jacob Loke, Pathophysiology and Treatment of Inhalation Injuries, 2020
K. Randall Young, Herbert Y. Reynolds
A number of investigators have noted that hyperoxia may augment other forms of lung injury. Rinaldo and co-workers (1984) examined the combined effect of endotoxemia and hyperoxia on rats, and found that previous exposure to 100% oxygen potentiated the development of neutrophil chemotactic activity in BAL fluid and accelerated and intensified the neutrophil alveolitis seen in these animals. The mechanism whereby hyperoxia worsened the endotoxin injury was not clear from their investigation.
Acute oxygen therapy: a cross-sectional study of prescribing practices at an English hospital immediately before COVID-19 pandemic
Published in Expert Review of Respiratory Medicine, 2021
Ravina Barrett, Eugene Catangui, Railton Scott
Appropriate prescribing of oxygen therapy can be potentially life-saving by reversing hypoxemia, by increasing oxygen delivery to tissues and subsequently preventing tissue hypoxia [1]. However, it is essential that clinicians acknowledge that oxygen is a drug with specific biochemical and physiologic actions, a distinct range of effective doses and well-defined adverse effects at escalating doses. The human body responds differently depending on the type of exposure to supplemental oxygen. Short exposures to high partial pressures at greater than atmospheric pressure leads to central nervous system toxicity, as seen in divers or in hyperbaric oxygen therapy. Pulmonary and ocular toxicity results from longer exposure to elevated oxygen levels at normal atmospheric pressure [2]. Recent research delineates the negative consequences associated with excessive oxygen supplementation, i.e. the physiological state of hyperoxia. Negative effects of hyperoxia include; absorption atelectasis, the formation of reactive oxygen species (ROS), reduced cardiac output and induction of cerebral, retinal, and coronary vasoconstriction [3,4].
Effects of long term normobaric hyperoxia exposure on lipopolysaccharide-induced lung injury
Published in Experimental Lung Research, 2020
Jick Hwan Ha, Sei Won Kim, In Kyoung Kim, Chang Dong Yeo, Hyeon Hui Kang, Sang Haak Lee
Prolonged exposure to hyperoxia is well known to cause oxygen toxicity and lung damage, particularly in animal models.10,12,13 Prolonged breathing of high oxygen levels causes hyperoxic acute lung injury, the severity of which is directly proportional to the inspired O2 fraction (FiO2) and duration of exposure.9 Most animals typically die after 3–6 days with respiratory failure under conditions of FiO2 ≥ 0.9–1.0.21 Several experiments have shown that oxygen toxicity rises more rapidly as FiO2 increases above 0.6 and exposure time is prolonged.9 However, few studies have been conducted on humans and there is no clear evidence that exposure to hyperoxia is toxic.11,15,16
Hyperbaric oxygen therapy in ophthalmic practice: an expert opinion
Published in Expert Review of Ophthalmology, 2020
Lawrence J. Lin, Tiffany X. Chen, Kenneth J. Wald, Andrea A. Tooley, Richard D. Lisman, Ernest S. Chiu
Future research involving controlled trials with more participants will help clarify best practices regarding HBOT usage. These studies should aim to elucidate the role of HBOT in ocular treatment and determine the optimal regimens of care. Further clarification of the prognostic factors will aid in the identification of specific patient subgroups that would benefit most from treatment. As we continue to enhance our understanding of the physiologic response to hyperoxia, we will be able to better identify therapeutic applications and limit adverse effects.