Sign in. EMS World Expo. Current Issue. Issue Archives. Start Print Subscription. Renew Print Subscription. Start Digital Subscription. Patient Care. Expo on Demand. CE Articles. Online Product Guide. Contact Us. Advisory Board. About Us. Kevin T. Copied to clipboard. Oxygen Absorption Adequate oxygen delivery and absorption is essential for proper function at the cellular, tissue and organ levels.
Box 1: Causes for increased oxygen demand Serious injury or illness Infection Surgery Pain Anxiety Cellular oxygen consumption depends on an adequate oxygen supply. Complications of Oxygen Delivery Like every other drug, oxygen administration has complications.
Box 2: Complications of oxygen delivery Skin breakdown and irritation Dry mucous membranes Oxygen toxicity Absorbative atelectasis Carbon dioxide narcosis Oxygen Toxicity Recall from earlier in this article that under high oxygen environments, cells metabolize oxygen more quickly.
Toxicity in Hyperbaric Medicine Hyperbaric oxygen therapy is an important tool in modern medicine for management in a variety of situations including diving emergencies, wound management and carbon monoxide toxicity. Neonatal Oxygen Administration A host of changes occur during and shortly after the birth of a neonate. References 1. Morton PG, et al, eds. Clinical Manifestations and Assessment of Respiratory Disease , 5 th edition.
Louis, MO: Elsevier, Circulation S—, Shapiro BA, et al. Clinical Application of Blood Gases, 5 th Edition. Circulation S—S, Ntoumenopolus G. Using titrated oxygen instead of high flow oxygen during an acute exacerbation of chronic obstructive pulmonary disease COPD saves lives. J Physiother 57 1 , Austin MA, et al. Effect of high flow oxygen on mortality in chronic obstructive pulmonary disease patients in prehospital setting: randomized controlled trial.
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But breathing pure oxygen can sometimes be necessary. Astronauts and deep-sea scuba divers sometimes breathe pure oxygen because they work in very dangerous places. Sick people, including premature babies in hospital or people in hospital with the coronavirus , might also need some extra help breathing.
It acts like a medicine to help calm and settle their breathing. Again, too much oxygen can be dangerous. So we need oxygen to help us get energy from our food. Initially, there are increased ROS and depleted antioxidant levels, and the lung fails to clear itself of mucous. The inflammation phase or exudative phase is characterized by the destruction of the pulmonary lining and migration of leukocyte derived inflammatory mediators to the sites of injury. The proliferative phase is subacute and there are cellular hypertrophy, increased secretions from surfactant secreting alveolar type II cells, and increased monocytes.
The final terminal phase is the fibrotic phase in which the changes to the lung are irreversible and permanent. There is collagen deposition and thickening of the pulmonary interstitial space and the lung becomes fibrotic [ 24 — 27 ]. Clinically, progressive hypoxemia, or high O 2 tension in the blood, requires increased FIO 2 and assisted ventilation, which further aggravate the pathophysiological changes associated with O 2 toxicity.
Chest X-rays may show an alveolar interstitial pattern in an irregular distribution with evidence of a moderate loss of volume from atelectasis, however there is no clinical way of diagnosing O 2 toxicity. Lung biopsy specimens may show changes consistent with O 2 toxicity but the primary value of the biopsy is to exclude other causes of lung injury.
Air pressure changes within the enclosed lung cavity and ventilator-induced injury may accompany and be indistinguishable from O 2 toxicity. The pulmonary cellular response to hyperoxic exposure and increased ROS is well described. Anatomically, the pulmonary epithelial surface is vulnerable to a destructive inflammatory response. This inflammation damages the alveolar capillary barrier leading to impaired gas exchange and pulmonary edema. Reactive O 2 species induces pulmonary cell secretion of chemoattractants, and cytokines stimulate macrophage and monocyte mobilization and accumulation into the lungs, leading to additional ROS.
The ROS leukocyte interaction further exacerbates injury. Research has shown that as these highly reduced cell layers become increasingly oxidized and levels of antioxidants fall, ROS-induced activation of multiple upstream signal transduction pathways regulates the cellular response: adaptation, repair, or cell death by apoptosis, oncosis, or necrosis [ 28 , 29 ]. The MAPK pathway is a regulator of cell death genes, stress, and transformation and growth regulation.
The AKT family of signals plays an important role in glucose metabolism, cell proliferation, apoptosis, transcription, and cell migration. These signaling pathways are regulators of the pulmonary epithelial cell response to increases in ROS and hyperoxia [ 18 , 34 ].
Cytokine and chemokine overexpression in response to hyperoxic stress can be protective. Oxygen is a requirement for cellular respiration in the metabolism of glucose and the majority of O 2 consumed by the mitochondria is utilized for adenosine triphosphate ATP generation [ 38 , 39 ]. The mitochondrial electron transport chain reduces the elemental molecular O 2 to ionic O 2 by the relay of electrons making O 2 usable for ATP generation, during this process, oxidizing free radicals are generated [ 40 , 41 ].
Toxic levels of O 2 lead to the formation of additional ROS, which can impose damage to lipid membranes, proteins, and nucleic acids. Reactive O 2 species mediate physiological and pathophysiological roles within the body [ 42 ].
Free radicals are a type of unstable, reactive, short-lived chemical species that have one or more unpaired electrons and may possess a net charge or be neutral.
The species is termed free because the unpaired electron in the outer orbit is free to interact with surrounding molecules [ 42 , 43 ]. Chemically, three types of reactions lead to the formation of ROS. The one-electron reduction of molecular O 2 to the superoxide anion is catalyzed by transition metals including iron Fe and copper Cu such as. The in biological membranes can act in four different modes: electron transfer, nucleophilic substitution, deprotonation, and a hydrogen atom abstraction as in.
A initiated Fenton-type reaction and the decomposition of H 2 O 2 requires and H 2 O 2 as precursors and Fe and Cu presence for completion. These ROS-producing reactions occur endogenously involving enzymes, neutrophils, and organelles such as the mitochondria and exogenously induced by radiation, pollutants, xenobiotics, and toxins. Cellular survival and adaptation in an oxidative atmosphere are dependent upon sufficient antioxidant defenses to counteract the effects of ROS on cells and tissues [ 48 ].
Oxidant antioxidant homeostasis is highly regulated and essential for maintaining cellular and biochemical functions [ 49 ]. A change in the balance toward an increase in the oxidant over the capacity of the antioxidant defines oxidative stress and can lead to oxidative damage.
Changing the balance toward an increase in the reducing power of the antioxidant can also cause damage and is defined as reductive stress [ 50 — 52 ]. Reduction, antioxidant and oxidation, or pro-oxidant reactions result from a gain or a loss of electrons and a loss or a gain in O 2 [ 50 , 53 , 54 ]. An antioxidant a reductant or reducing agent is anything that can prevent or inhibit oxidation [ 55 — 57 ].
Delay of oxidation can be achieved by preventing the generation or inactivating ROS [ 58 ]. Prevention, diversion, dismutation decay , scavenging, and quenching are specialized antioxidant properties Table 1. Antioxidant defenses may be classified as nonenzymatic and enzymatic or endogenous and dietary. Examples of nonenzymatic antioxidants are glutathione GSH , ascorbic acid, vitamin E, beta-carotene, and uric acid. Endogenous or dietary antioxidants are based on the ability of the antioxidant to be synthesized by humans.
Dietary antioxidants are ascorbic acid, vitamin E, and beta-carotene [ 59 , 60 ]. Antioxidants can be classified into four categories based on function. Superoxide dismutase converts to H 2 O 2 and has three isoforms widely distributed in mammalian organisms. The protective effects of EcSOD in the lungs are extremely important and well-established [ 65 — 68 ].
Catalase, one of the most potent catalysts found mostly in the peroxisome, functions to decompose H 2 O 2 to H 2 O. Catalase defense from oxidant injury to lung epithelial cells exists in the cytosol or the mitochondria. Glutathione reductase is an important antioxidant enzyme for maintaining the intracellular reducing environment.
Glutathione disulfide is produced through the oxidation of GSH by ROS that arise during conditions of oxidative stress. The damaging effects of hyperoxia can lead to O 2 toxicity, cell death, and can be a triggering factor in ALI [ 22 ].
Acute lung injury and acute respiratory distress syndrome ARDS are secondarily occurring, inflammatory syndromes caused by triggers or risk factors described as direct or indirect, pulmonary or extrapulmonary. The pathological changes associated with HALI mimic the ALI triggered by other conditions such as hemorrhagic shock, reperfusion injury, pneumonia, sepsis, or paraquat inhalation [ 23 , 33 , 74 , 75 ].
The risk of developing ALI or ARDS after inhalation injury is dependent on the toxicity and concentration of the inhaled substance [ 17 ]. For example, the cells and structure of the alveolar capillary membrane are highly susceptible to damage by toxic levels of O 2 [ 76 ]. The ratio between arterial pressure of O 2 PaO 2 and the FIO 2 concentration delivered by ventilator support distinguishes the two syndromes.
The injury to the alveolus is thought to develop when pulmonary or systemic inflammation leads to systemic release of cytokines and other proinflammatory molecules. Mast cells, which express mediators that exert effects on lung vasculature, are also increased after hyperoxic exposure [ 78 ]. Cytokine release activates alveolar macrophages and recruits neutrophils to the lungs.
Subsequent activation of leukotrienes, oxidants, platelet activating factor, and protease occurs. These substances damage capillary endothelium and alveolar epithelium, disrupting the barriers between the capillaries and air spaces. Edema fluid, proteins, and cellular debris flood the air spaces and interstitium, causing disruption of surfactant, airspace collapse, ventilation-perfusion mismatch, shunting, and stiffening of the lungs with decreased compliance and pulmonary hypertension.
There is no pattern to the injury; however, dependant lung areas are most frequently affected [ 74 , 79 ]. Tissue examination reveals that surfactant disruption, epithelial injury, and sepsis initiate the increased expression of cytokines that sequester and activate inflammatory cells.
Increased release of ROS alters normal endothelial function. Microarray analysis has revealed increased expression of genes related to oxidative stress, antiproteolytic function, and extracellular matrix repair as well as decreased surfactant proteins in ozone-induced ALI [ 80 ]. Diffuse alveolar damage results with intra-alveolar neutrophils indicating the presence of an inflammatory response in the alveoli.
Red blood cells, cellular fragments, and eroded epithelial basement membranes are present with formation of hyaline membranes, indicating that serum proteins have entered and precipitated in the air spaces due to disruption of the alveolar capillary barrier.
Formation of microthrombi indicates the presence of endothelial injury and activation of the coagulation cascade [ 81 ]. Acute lung injury syndrome presents within 24 to 48 hours after the direct or indirect trigger.
Initially, the patient may experience dyspnea, cough, chest pain, tachypnea, tachycardia, accessory muscle use, cyanosis, mottled skin, and abnormal breath sounds crackles, rhonchi, and wheezing.
Blood gas analysis reveals progressive worsening of hypoxemia, leading to respiratory failure. Bilateral infiltrates are seen on a chest X-ray and are consistent with pulmonary edema but without the cardiac component of elevated left atrial pressure.
Treatment includes mechanical ventilation, supportive care, and treatment of the underlying causes [ 16 ]. Oxygen, often used to treat hypoxemia in the clinical setting, is itself a triggering factor in HALI given that the exposure is sufficiently concentrated and of adequate duration. The lung is a vulnerable target for oxidant-induced injury, initiating a cascade of protein signals that determine the cellular response.
The alveolar epithelial and alveolar capillary endothelial surfaces are injured. Hyperpermeability, microthrombi resulting from altered coagulation and fibrinolysis , collagen deposition, and fibrosis alter alveolar structure and function. Understanding precise mechanisms of injury and pulmonary cellular responses to hyperoxia is essential evidence for expert practice.
The information or content and conclusions do not necessarily represent the official position or policy of, nor should any official endorsement be inferred by, the TSNRP, the Department of Defense, or the US Government. Mach et al. Purchase access.
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