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- 1. Hypoxia By (Dr. Taher FT Elshami) 2016 Matric number: G1515929
- 2. Outline Definition ofhypoxia Causes of Hypoxia Effects of Hypoxia Types of Hypoxia Hypercapnia Oxygen therapy
- 3. HYPOXIA: Acondition in which the oxygen available is inadequate at the tissue level A pathological condition in which the body as a whole (generalized hypoxia) or a region of the body (regional hypoxia) is deprived of adequate oxygen supply
- 4. Causes of Hypoxia Inadequate oxygenation -Deficiency of oxygen in atmosphere - Hypoventilation (neuromuscular disorders) Venous-to-arterial shunts (right-left cardiac shunts) - Eisenmenger's syndrome Pulmonary disease - Hypoventilation due to increased airway resistance or decreased compliance - Abnormal VA/Q ratio - Diminished respiratory membrane diffusion
- 5. Inadequate oxygentransport to tissues - Anaemia or abnormal Hb - General circulatory deficiency - Localized circulatory deficiency - Tissue oedema Inadequate tissue capability of using oxygen - Poisoning of cellular oxidation enzymes - Diminished cellular metabolic capacity for using oxygen, because of toxicity, vitamin deficiency or other factors
- 6. Effects of Hypoxiaon body • Hypoxia, if severe - can cause death of cells throughout the body • In less severe degrees - Depressed mental activity, sometimes results in coma - Reduced work capacity of muscles
- 7. Types of Hypoxia 1.Atmospheric Hypoxia (Hypoxic Hypoxia) 2. Hypoventilation Hypoxia 3. Anemic Hypoxia 4. Circulatory or ischemic Hypoxia 5. Histotoxic or cytotoxic Hypoxia
- 8. Atmospheric Hypoxia (HypoxicHypoxia) • An insufficient O2 supply reaches the blood • Due to: - Decreased atmospheric PO2 at high altitudes - Reduced alveolar ventilation like Chronic obstructive pulmonary disease (COPD) - Impaired alveolar gas exchange 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
- 9. Hypoventilation Hypoxia Areduced amount of air enters the alveoli in your lungs, resulting in hypoxia and hypercapnia COPD Scoliosis, nasal septum deformation Weakened respiratory muscles - motor neurone disease
- 10. Anemic Hypoxia • ReducedO2-carrying capacity of blood • Due to decreased total Hb or RBC Anemia Carbon monoxide poisoning Methemoglobinemia Sickle Cell Anemia Treatment involves blood transfusions, hyperbaric chamber, bone marrow transplant
- 11. Circulatory or ischemicHypoxia Insufficient O2 reaches the tissue due to reduced blood flow Systemic or local 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 patient is hypoxic Cardiovascular instability or failure Shock Arrhythmias Treatment include increasing cardiac output with use of cardiovascular drugs and therapy, supplemental oxygen
- 12. Histotoxic or cytotoxicHypoxia Impaired utilization of O2 by the tissues despite a sufficient supply of O2 in the mitochondria Cyanide Poisoning will inhibit cellular metabolism from occuring; the cells can not process the O2 Treatment: Reversal of poisoning, supplemental oxygen and/or ventilation 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.
- 13. Hypercapnia Excess carbondioxide (CO2) in the body (> 45 mm Hg in blood) Associated with hypoxia - Hypoventilation - Circulatory deficiency Hypoxia caused by reduced availability of O2
- 14. • Flushed skin •Full pulse • Tachypnea • Dyspnea • Muscle twitches • Hand flaps • Reduced neural activity • Raised blood Hypercapnia – Symptoms & signs
- 15. Raised PCO2 •60 to 75 mm Hg – air hunger (rapidly & deeply) - Dyspnea • 80 to 100 mm Hg – lethargic & semicomatose • 120 to 150 mm Hg – anesthesia and death
- 16. Oxygen therapy Goals ofoxygen therapy: 1. Correcting Hypoxemia By raising Alveolar and Blood levels of Oxygen Easiest objective to attain and measure 2. Decreasing symptoms of Hypoxemia Supplemental O2 can help relieve symptoms of hypoxia Lessen dyspnoea/work of breathing Improve mental function
- 17. 3. Minimizing Cardiopulmonaryworkload Cardiopulmonary system will compensate for Hypoxemia by: Increasing ventilation to get more O2 in the lungs and 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 and Pulmonary Hypertension These cause an increased workload on the right side of heart Over time the right heart will become more muscular and then eventually fail (Cor Pulmonale)
- 18. Supplemental O2can relieve hypoxemia and relieve pulmonary vasoconstriction and 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%
- 19. Classification of O2therapy devices Oxygen delivery systems Low flow systems High flow systems
- 20. Low flow O2delivery 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.
- 21. High flow O2delivery 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.
- 22. Indications for O2therapy: 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.
- 23. Precautions and Hazards O2 Toxicity Primarily affects Lungs and CNS 2 determining factors of O2 toxicity PO2 Time of exposure i.e., higher the PO2 and 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
- 24. Pathophysiology High PO2 damagescapillary endothelium Followed by interstitial edema and AC membrane thickening Type I cells are destroyed (cells that create new lung tissue, gas exchange cells) Type II cells proliferate (trigger inflamatory response)
- 25. Exudative phase Alveolar fluidbuildup (from inflamatory response) leads to low ventilation/perfusion ratio (shunting) hypoxemia Hyaline membranes form alveolar level Proteinaceous eosinophilic (basic) material Composed of cellular debris and condensed plasma proteins. Pulmonary fibrosis develop Pulmonary Hypertension develops
- 26. Treatment: Try to keeppatient alive while reducing FiO2 Cause: Overproduction of O2 free radicals By products of cellular metabolism Toxic in excessive amounts Normally antioxidants and other special enzymes dispose of excess free radicals Neutrophils (WBC’s) and macrophages flood the infiltrate the tissue and mediate inflammation response, leading to more free radicals
- 27. References Ganong, W.F. (2005) Singapore .The MacGrow-Hill Companies, Inc Sherwood, L. (2015). Human physiology: from cells to systems. Cengage learning. Patel, D. N., Goel, A., Agarwal, S., Garg, P., & Lakhani, K. K. (2003). Oxygen Toxicity. JIACM, 4(3), 234–7. COLLEGE OF RESPIRATORY THERAPISTS OF ONTARIO C L I N I C A L B E S T P R A C T I C E G U I D E L I N E O x y g e n T h e r a p y Oxygen Therapy Clinical Best Practice Guideline. (2013).