hypoxia and oxygen therapy
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- 1. Hypoxia and oxygen therapy
2. Historical considerations Carl Wilhelm Scheele 1773 Discovered O2 John Pristley 1774 Was the first to publish a paper on O2 Antoine Lavoisier 1777 Coined the term O2 3. Oxygen: Colourless Odourless Tasteless Transparent gas Slightly heavier than air Constitues 20-21% of atmospheric air Essential for life 4. Importance of O2 in cell chemistry Required in aerobic metabolism for: 1. Production of high energy phosphate compounds (ATP) 2. Dehydrogenation of flavo proteins 3. Biotransformation of drugs 4. Oxidation of certain other substrates.. 5. Definations: Hypoxia: low level of oxygen at tissue level Hypoxemia: low levels of oxygen in blood Partial pressure: the pressure exerted on a surface by the molecules of individual gases. The partial pressure of oxygen can be calculated for a given atmospheric pressure, by multiplying concentration of a gas by the atmospheric or barometric pressure. Eg: 760 mm Hg 21% = 160 mm Hg 6. Oxygen cascade Oxygen cascade refers to the progressive decrease in the partial pressure of oxygen from the ambient air to the cellular level. PO2 in inspired air 150-160 mm Hg PO2 in alveolar gas (PAO2) 100- 110 mm Hg PO2 in arterial blood (PaO2) 98 mm Hg PO2 in Capillary blood 50-80 mm Hg PO2 in tissues 30- 50 mm Hg PO2 in cell mitochondria 10- 20 mmHg 7. Factors affecting oxygenation at various levels in O2 cascade: Partial pressure Affected by: Inspired oxygen PiO2 Barometric pressure PB Oxygen concentration FiO2 Alveolar gas PAO2 Oxygen consumption VO2 Alveolar ventilation VA Arterial blood PaO2 Dead space ventilation Increased V/Q Shunt Decreased V/Q Cellular PO2 Cardiac output CO Hemoglobin Hb 8. Oxygen therapy Goals of oxygen therapy: 1. Correcting Hypoxemia By raising Alveolar & Blood levels of Oxygen Easiest objective to attain & measure 2. Decreasing symptoms of Hypoxemia Supplemental O2 can help relieve symptoms of hypoxia Lessen dyspnoea/work of breathing Improve mental function 9. 3. Minimizing Cardiopulmonary workload Cardiopulmonary system will compensate for Hypoxemia by: Increasing ventilation to get more O2 in the lungs & to the Blood Increased work of breathing Increasing Cardiac Output to get more oxygenated blood to tissues Hard on the heart, especially if diseased Hypoxia causes Pulmonary vasoconstritcion & Pulmonary Hypertension These cause an increased workload on the right side of heart Over time the right heart will become more muscular & then eventually fail (Cor Pulmonale) 10. Supplemental o2 can relieve hypoxemia & relieve pulmonary vasoconstriction & Hypertension, reducing right ventricular workload!! At our institution, minimal acceptable saturation for post surgical patients who are cared for in non critical setup is 92% 11. Assessing the need for oxygen therapy 3 basic ways: Laboratory measures invasive or noninvasive PAO2, PaO2, SaO2, SpO2 monitoring Clinical Problem or condition postoperative patients, pneumonia, atelectasis, pulmonary edema, etc Symptoms of hypoxemia Eg: tachycardia, tachypnoea, hypertension, cyanosis, dyspnoea, disorientation, clubbing, etc 12. Methods of oxygen administration Method selection depends upon required concentration of oxygen. However, during oxygen therapy the relative dangers of hypoxia and O2 toxicity should be kept in mind. Criteria for selecting the method: 1. Patients GCS and patients comfort 2. Level & range of FiO2 required 3. Extent of humidification required 13. Classification of O2 therapy devices Oxygen delivery systems Low flow systems High flow systems 14. Low flow O2 delivery system Flow does not meet inspiratory demand Oxygen is diluted with air on inspiration These devices have limited reservoir to store oxygen and are unable to deliver consistent inspired oxygen concentrations in settings of varying respiratory rates & tidal volumes. 15. Nasal prongs: 16. Simple face masks: 17. High flow O2 delivery system: Supplies given FiO2 at flow rates higher than inspiratory demand. They are suitable for delivering consistent and predictable concentrations of oxygen. Uses entrainment of air to maintain oxygen supply. Eg: venturi mask, non rebreathing mask, puritan face mask. 18. Air Entrainment system Amount of air entrained varies directly with: port size Velocity The more air entrained: Higher flow Lower FiO2 19. Venturi mask: 20. Non rebreathing mask with reservoir mask: 21. Indications for O2 therapy: Arterial PO2 < 60 mmHg or SaO2 < 90% Cardiac & respiratory arrest Respiratory failure Cardiac failure or myocardial infarction Shock of any cause Increased metabolic demands (eg. Burns, multiple injuries, severe sepsis) Post operative state Carbon monoxide poisoning. 22. Hypoxia HYPOXIA: A condition in which the oxygen available is inadequate at the tissue level Five types of hypoxia: Anemic Hypoxemic Histotoxic Circulatory Hypermetabolic 23. Anemic Hypoxia Having a decreased carrying capacity for oxygen, the pt with decreased or abnormal Hb Anemia Carbon monoxide poisoning Methemoglobinemia Sickle Cell Anemia Treatment involves blood transfusions, hyperbaric chamber, bone marrow transplant 24. Hypoxemic Hypoxia Low PAO2 due to the atmosphere Hypoventilation PCO2 is rising Diffusion Defects The PaO2 will be lower in all cases, but the PCO2 may or may not be increased. Treatment: Compensatory actions to reduce inequalities, supplemental oxygen 25. Histotoxic Hypoxia Inability for tissues to utilize oxygen available Cyanide Poisoning will inhibit cellular metabolism from occuring; the cells can not process the O2 Treatment: Reversal of poisoning, supplemental oxygen and/or ventilation 26. Circulatory Hypoxia A decrease in cardiac output results in a low BP and a prolonged systemic transit time The PaO2 can be high, but because of the time it takes to get to the tissues, the pt is hypoxic Cardiovascular instability or failure Shock Arrhythmias Treatment include increasing cardiac output with use of cardiovascular drugs and therapy, supplemental oxygen 27. Hypermetabolic Hypoxia In some disease states the body requires a slight increase in metabolism (i.e. wound healing requires 5% increase) Extensive burns and some cancers will cause large increases metabolism to the point that supplemental O2 is required Treatment: Supplemental O2 or FiO2 28. Approach to selecting appropriate O2 delivery system: Purpose (Objective) Increase FiO2 to correct hypoxemia minimize symptoms of hypoxemia Minimize Cardiopulmonary workload Patient Cause & severity of hypoxemia Age Neuro status/orientation Airway in place/protected Regular rate & rhythm (minute Ventilation) Equipment Performance The more critical, the greater need for high stable FiO2 Becomes more difficult the more critical due to pt varying pattern 29. Pt Categories Emergency Highest FiO2 possible Highest PaO2 possible Critical Adult >60% O2 PaO2 >60mmHg SpO2 >90% Stable adult, acute illness, mild hypoxemia Low to moderate FiO2 Response to therapy, not precise concentrations 30. Chronic dz adult, acute on chronic illness Ensure adequate oxygenation without depressing Ventilation SpO2 85-90% PaO2 50-60mmHg Use ventilating mask to control FiO2 precision 31. Assess response to therapy!! If not maintainable on Cannula, use masks Pt may remove mask frequently due to Discomfort Convenience Change in mental status Encourage Cannula use between mask use if mask must come off for periods 32. Precautions & Hazards O2 Toxicity Primarily affects Lungs & CNS 2 determining factors of O2 toxicity PO2 Time of exposure i.e., higher the PO2 & exposure time the greater the toxicity. CNS effects occur with Hyperbaric Pressures Pulmonary effects can occur @ clinical PO2 levels Patchy infiltrates on x-ray, prominent in lower lung fields Major alveolar injury 33. Pathophysiology High PO2 damages capillary endothelium Followed by interstitial edema & AC membrane thickening Type I cells are destroyed (cells that create new lung tissue, gas exchange cells) Type II cells proliferate (trigger inflamatory response) 34. Exudative phase Alveolar fluid buildup (from inflamatory response) leads to low ventilation/perfusion ratio (shunting) hypoxemia Hyaline membranes form @ alveolar level Proteinaceous eosinophilic (basic) material Composed of cellular debris & condensed plasma proteins. Pulmonary fibrosis develop Pulmonary Hypertension develops 35. Treatment: Try to keep pt alive while reducing FiO2 Cause: Overproduction of O2 free radicals Byproducts of cellular metabolism Toxic in excessive amounts Normally antioxidants & other special enzymes dispose of excess free radicals Neutrophils (WBCs) & macrophages flood the infiltrate the tissue & mediate inflammation response, leading to more free radicals 36. How much is too much? >50% for very extended times >PO2 the less time it takes Goal of ideal oxygen therapy: Use the lowest FiO2 possible to maintain adequate tissue oxygenation 37. Other side effects Growing lungs are more sensitive to O2 Retinopathy of Prematurity (ROP), more later Bronchopulmonary Dysplasia (BPD), chronic lung dz, Absorption Atelectasis, Fire hazards, etc Depression of Ventilation Hypercarbic drive is blunted High PCO2 no longer stimulates pt to increase Ventilation Suppression of hypoxic drive The only stimulus left to increase Ventilation is due to hypoxia 38. When you add to much O2, (remove the hypoxia) you effectively remove the neurological stimulus to breathe. (peripheral chemoreceptors) Hypoventilation occurs CO2 continues to elevate to sedative levels Pt stops breathing until hypoxic again If CO2 is too high, they will remain sedated & causes Cardiopulmonary arrest Never withhold O2 therapy from a Hypoxic pt (PaO2) 39.