Methods in Experimental Pathology of Pulmonary Vasculature
Joan Gil in Models of Lung Disease, 2020
Perhaps no injury or adaptation by lung is without an effect on its vessels. Here we have selected a few examples to illustrate interpretation of injury, its pathophysiology, or pathogenesis, and always with a focus on structure. Hypoxia offers an example of vasoconstriction, metabolic perturbation, and structural remodeling that includes even a change in cell phenotype. Inflammation represents the humoral and cellular response to a variety of injuries and includes a variety of changes calling for structural interpretation. Adult respiratory failure (ARF) and the adult respiratory distress syndrome (ARDS) exemplify acute alveolar damage and its progression. Hyperoxia is doubly linked with this since it contributes to the lung appearance of fatal cases. While it is a life-saving treatment, it also causes significant injury. It is included here because it provides an example of both a necrotizing lesion in its early phases and structural adaptations in the healing phase. It illustrates several important biological concepts of injury, adaptation, and repair, and is relevant to disease of all ages: adult, child, and newborn. Bronchopulmonary dysplasia is discussed as an example here of both hyperoxic injury and its impairment of lung growth.
Oxygenation
Hemanshu Prabhakar, Charu Mahajan, Indu Kapoor in Manual of Neuroanesthesia, 2017
Ensuring adequate delivery of oxygen is crucial in perioperative patient management. The clinician must seek to achieve a balance between the deleterious extremes of hypoxemia and hyperoxia. The harmful effects of hypoxemia are well-established and warrant special consideration in neurosurgical patients, especially in those who have sustained a brain injury and are at risk for compromised cerebral blood flow (CBF). However, indiscriminate use of increased inspired oxygen fractions can lead to detrimental consequences as well, particularly with regard to pulmonary function and central nervous system toxicity. This chapter discusses the rationale for administering increased oxygen concentrations in neurosurgical and non-neurosurgical patients alike, as well as the harms of doing so. We also comment on high-acuity situations in neurosurgery and neurocritical care, and how tailoring oxygen therapy in these populations can affect patient outcomes.
Pulmonary Lymph and Lymphatics
Waldemar L. Olszewski in Lymph Stasis: Pathophysiology, Diagnosis and Treatment, 2019
Prolonged inhalation of 100% oxygen may be damaging to the membranes.134,136 Breathing pure oxygen at one atmosphere of barometric pressure results in elevation of lung tissue oxygen tension to levels that approach 700 mmHg, whereas oxygen tension in other tissue changes minimally. This may explain the specificity of oxygen toxicity for the lung.137 Changes in the metabolic activity of pulmonary endothelial cells may occur resulting in impaired clearance of 5-hydroxytryptamine and prostaglandins and reduced activity of angiotensin converting enzyme.139,140 The latter reflects endothelial injury associated with interstitial edema. Such changes are followed by accumulation of platelets and neutrophils with destruction of endothelial and type I epithelial cells.141 Sublethal doses of oxygen may be followed by proliferation of type II pulmonary epithelial cells and interstitial fibrosis. Hyperoxia increases the production of free oxygen radicals which may be one mechanism of toxicity to the lung.142
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
Determination of carboxyhemoglobin half-life in patients with carbon monoxide toxicity treated with high flow nasal cannula oxygen therapy
Published in Clinical Toxicology, 2019
Ibrahim Ulas Ozturan, Elif Yaka, Selim Suner, Asim Enes Ozbek, Cansu Alyesil, Nurettin Ozgur Dogan, Serkan Yilmaz, Murat Pekdemir
This study has a number of limitations. First, the study is not a comparison study but consists of only one treatment arm. Therefore, direct comparison of oxygen delivery by HFNC and standard nonrebreather face mask or endotracheal tube cannot be made. Second, because the aim of the study was not a clinical efficacy assessment, we did not follow patients after their ED visit. Therefore, possible delayed complications of CO toxicity and potential long-term toxicity from hyperoxia could not be determined. Third, although all patients had signs of acute CO toxicity, the source of CO was not recorded in 14 patients. Information regarding ambient concentration of CO and the duration of exposure was not available. COHb half-life may be influenced by the concentration and duration of exposure to CO.
Related Knowledge Centers
- Molecule
- Oxygen
- Oxygen Toxicity
- Reactive Oxygen Species
- Tissue
- Hypoxia
- Lung
- Partial Pressure
- Pulmonary Alveolus
- Gas Blending