The Use of Hyperoxia in the Treatment of Respiratory Failure

Introduction

An essential and fundamental gas for maintaining human existence is oxygen. The atmosphere has had oxygen since five billion years ago. The damaging effects of oxygen were initially identified by Priestley. In individuals with respiratory failure, oxygen can be given as recommended and have positive therapeutic effects. A sickness known as respiratory failure occurs when the respiratory system is unable to maintain a sufficient gas exchange while at rest or during activity. Inability to properly carry out the vital tasks of breathing, which include eliminating carbon dioxide and delivering oxygen to the blood. Oxygen is required as the main therapy for patients with respiratory failure to treat hypoxemia. Prescriptions for oxygen supplementation must be accurate and in line with indications in order to prevent excessive oxygen consumption. Hyperoxia and oxygen poisoning can result from excessive oxygen exposure. Acute (sudden) and chronic (slow) respiratory failure are the two types of respiratory failure. Acute respiratory failure is respiratory failure that happens in people who had healthy lungs before the sickness started. On the other hand, people with long-term lung conditions including emphysema and chronic bronchitis will experience chronic respiratory failure. Patients can handle steadily worsening hypoxia and hypercapnia. Acute respiratory failure can be brought on by both extra pulmonary and intrapulmonary problems. Abnormalities in the lower respiratory tract, pulmonary circulation, interstitial tissue, and alveolar capillaries are examples of intrapulmonary diseases. The respiratory center, the neuromuscular system, the pleura, and the upper airway all exhibit extra pulmonary abnormalities.

Hyperoxia

Due to the increased oxygen concentration during inspiration, ambient pressure, or both, oxygen has a harmful impact at high partial pressures. Particularly in preterm newborns, oxygen poisoning can cause symptoms in the central nervous system, lungs, and eyes. Depending on the oxygen concentration and the time spent administering oxygen, different levels of toxicity develop at different times. Treatment of the symptoms of oxygen toxicity is necessary for prevention and early detection. An excessive amount of oxygen in the tissues and organs is known as hyperoxia. When the alveolar partial pressure of O2 (PaO2) is higher than what is normally breathed, oxygen poisoning ensues. There was a significant influx of ROS created in the pathogenic state of hyperoxia. Three different forms of ROS, including superoxide anion, hydrogen peroxide, and hydroxyl radical, are created when oxygen is reduced to water by the addition of four extra electrons. Overexposure to O2 is what causes the rise in ROS in intracellular and extracellular systems, upsetting the equilibrium between oxidants and antioxidants. Cells and tissues may become harmed as a result of this disruption of homeostasis. Many immune cells participate in the lung's reaction to hyperoxia.

Lung Toxicity

During prolonged oxygen exposure, lung toxicity consequences start to show. A latency period precedes the onset of symptoms, and the length of this time shortens with increasing PO2. Oxygen poisoning can cause cataracts, progressive and reversible myopia, and a reversible shortening of the peripheral visual field of the eye.

When the entire eye is exposed to high-pressure oxygen, such as when oxygen is delivered via a facemask, ocular consequences are to be expected. High oxygen exposure in neonates and premature infants results in retinopathy, chronic lung disease, and intraventricular hemorrhage. A larger risk, around 60%, exists for premature infants with a gestational age of less than 30 weeks or birth weight. Hyperoxia has the potential to harm alveolar epithelium and alveolar capillary endothelial cells. In hyperoxia-induced acute lung injury (ALI) settings, pulmonary microvascular hyperpermeability leads to the extravasation of plasma into the alveoli, which can result in pulmonary oedema, coagulation problems, and fibrin deposits in the fibrinolysis pathways. Oxygen free radicals harm type II alveolar epithelial cells, causing surfactant synthesis to be disrupted.

Journal Information

Journal of Pulmonology, an official publication of the Pulsus group, is a peer-reviewed, open-access journal in the respiratory research fraternity facilitating real-time peer-reviewed information on the subject. 

We accept articles across the discipline but are not limited to:

Asthma, Bronchiectasis, Bronchitis, Chronic Obstructive Pulmonary Disease (COPD), Chronic Hypercapnic respiratory failure (CHRF), Emphysema, Interstitial Lung Diseases, Lung Cancer, Obstructive Sleep Apnea, Pleural Effusion, Pneumoconiosis, Pneumonia, ARDS (acute respiratory distress syndrome), Cystic Fibrosis, Solitary Pulmonary Nodule, Tuberculosis. 

*The “Journal of Pulmonology”

Publishes current research articles related to Pulmonary.

Manuscript Submission link: https://www.pulsus.com/submissions/pulmonology.html