Oxygen Toxicity and physiological aspects.pptx

This document discusses the following about O2 toxicity
1. Defintion
2. Risk Factors
3. Pathophysiology
4. Management
5. Complications

1. Oxygen toxicity Presented by – Smrithi Rajeev M.Sc. Respiratory Therapy

2. Oxygen is one of the most widely available and used therapeutic agents in the world. It is a prescribable drug with specific biochemical and physiologic actions, a distinct range of effective doses and well-defined adverse effects at high doses. The human body is affected in different ways depending on the type of exposure. Short exposures to high partial pressures at greater than atmospheric pressure lead to central nervous system toxicity, most commonly seen in divers or in hyperbaric oxygen therapy. Pulmonary and ocular toxicity results from longer exposure to elevated oxygen levels at normal atmospheric pressure.

3. Defintion Oxygen toxicity, also known as oxygen poisoning, occurs when someone breathes oxygen at a higher than normal partial pressure This can lead to hyperoxia - a state of excess oxygen supply in tissues and organs. Oxygen toxicity can occur in two main clinical settings: Acute: The patient is exposed to high concentrations of oxygen for a short time. Chronic: The patient is exposed to lower concentrations of oxygen for a longer time

4. Risk factors Hyperbaric oxygen therapy patients Patients exposed to prolonged high levels of oxygen Premature infants Underwater divers.

5. Oxidative damage to cell membranes leads to the collapse of the alveoli in the lungs. Pulmonary effects can present as early as within 24 hours of breathing pure oxygen. Symptoms include pleuritic chest pain, substernal heaviness, coughing, and dyspnea secondary to tracheobronchitis and absorptive atelectasis, which can lead to pulmonary edema. Pulmonary symptoms typically abate 4 hours after cessation of exposure in the majority of patients.

6. CNS effects manifest with a multitude of potential symptoms. Early symptoms and signs are quite variable, but the twitching of the perioral and small muscles of the hand is a fairly consistent feature. If exposure to oxygen pressures is sustained, tinnitus, dysphoria, nausea, and generalized convulsions can develop. CNS toxicity is expedited by factors such as raised PCO2, stress, fatigue, and cold

7. The phenomenon of pulmonary toxicity is commonly referred to as the Smith effect. This can occur after prolonged exposure to oxygen greater than 0.5 ATA. The incidence of displaying pulmonary symptoms with oxygen toxicity is 5%. Preterm newborns are at distinct risk for bronchopulmonary dysplasia and retrolental fibroplasia with prolonged exposure to high concentrations of oxygen

8. pathophysiology Oxygen-derived free radicals have been proposed as being the probable etiological cause in the development of oxygen toxicity. Free radicals are generated due to the mitochondrial oxidoreductive processes and also induced by the function of enzymes such as xanthine/urate oxidase at extra-mitochondrial sites, from auto-oxidative reactions, and by phagocytes during the bacterial killing. These free radicals create lipid peroxidations , especially in the cell membranes, subdue nucleic acids and protein synthesis, and mollify cellular enzymes.

9. Continued exposure to high concentrations of oxygen results in heightened free radical production. This may damage the pulmonary epithelium, inactivate the surfactant, form intra-alveolar edema, interstitial thickening, fibrosis, and ultimately lead to pulmonary atelectasis

10. histopathology Oxygen toxicity stimulates the development of histological changes in the lung. This consists of pulmonary edema, congestion, intra-alveolar hemorrhage, and pulmonary injury. Tissue examination reveals that surfactant interruption and epithelial injury initiate the expanded expression of cytokines that activate inflammatory cells. The heightened release of oxygen free radicals modifies normal endothelial function. Microscopic examination at high magnification display the alveoli in the lung filled with smooth to slight floccular pink material characteristic of pulmonary edema and congestion. The capillaries in the alveolar walls are congested with many red blood cells.

11. Depression of ventilation In patients with chronic CO2 retention (e.g., COPD), high oxygen levels can increase PaCO2. This is partly caused by the Haldane effect, which increases the unloading of CO2 from the hemoglobin. It is also caused by an improvement in blood flow to lung units that are not well ventilated. As increased oxygen relaxes pulmonary vasoconstriction to these units, CO2 may increase. Less likely but still possible is a suppression of the hypoxic drive to breathe. However, in mechanically ventilated COPD patients, this should not be a problem when adequate alveolar ventilation is maintained

12. toxicokinetic 100% oxygen can be tolerated at sea level for about 24-48 hours without any severe tissue damage. Lengthy exposures produce definite tissue injury. There is moderate carinal irritation on deep inspiration after 3 to 6 hours of exposure of 2 ATA, extreme carinal irritation with uncontrolled coughing after 10 hours, and finally, chest pain and dyspnea ensue. In a majority of patients, these symptoms subside 4 hours after cessation of exposure.

13. History and physical examination Symptoms may include disorientation, breathing problems, and visual changes such as myopia and cataract formation. System-based signs and symptoms include the following. Central nervous system Headache Irritability and anxiety Dizziness Disorientation Hyperventilation Hiccups Cold shivering Fatigue Tingling in the limbs Visual changes such as blurring and tunnel vision Tinnitus and Hearing disturbances Nausea Twitching Tonic- clonic seizure

14. Pulmonary toxicity Mild tickle sensation on inhalation Mild burning on inhalation Uncontrollable coughing Haemoptysis Dyspnoea Rales Fever Hyperaemia of the nasal mucosa CXR shows inflammation and pulmonary edema

15. Eyes In premature babies, retinopathy of prematurity / retrolental fibroplasia Retinal edema Cataract formation (long-term) exposure

16. management Reduce exposure to increased oxygen levels For hyperbaric oxygen treatments, those at high risk may benefit from anti-epileptic therapy, prolonged air breaks, and limited treatment pressure. If an FIO2 of greater than 0.6 is required, then other techniques, such as PEEP, should be instituted. The improvement in oxygenation that occurs when PEEP is initiated often allows the FIO2 to be reduced. Prone positioning may also be of value

17. complications Tonic clonic convulsions Amnesia Tracheobronchtis Absorptive atelectasis Reversible myopia Delayed cataract formation In children, retrolental fibroplasia

18. Differential diagnosis Carbon dioxide narcosis Carbon monoxide poisoning Seizure disorder Migraine Multiple sclerosis

19. References Cooper JS, Phuyal P, Shah N. Oxygen Toxicity. [Updated 2023 Aug 1]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK430743/ Louise Thomson, James Paton, Oxygen Toxicity, Pediatric Respiratory Reviews, Volume 15, Issue 2, 2014, Pages 120-121 Pilbeams ; chapter 17; Page no 339; Effects of Positive Pressure Ventilation on the Pulmonary System – Hazards of Oxygen Therapy with Mechanical Ventilation