1. Oxygen Therapy By Dr. Yasser Moustafa Assist. Prof.Pulmonology Ain Shams University

2. Tissue Oxygenation FiO2 FiO2 Ventilation: Ventilation: –Resp Center –Airway –Alveoli ↓ PaO2 –Pillows: Ms – Bones Diffusion Diffusion Perfusion Perfusion CVS: CVS: –COP –Volume –Peripheral circulation Hb: Bind - Release Hb: Bind - Release –Anemia ↓ O2 Delivary –Abnormal ex CarboxyHb –2,3 DPG Utilization by cell: Utilization by cell: –Cyanide poisoning

3. Tissue Oxygenation Important Facts Normal PO2 in arterial blood (PaO2) ≥ 95mmHg: decrease with age. Normal PO2 in arterial blood (PaO2) ≥ 95mmHg: decrease with age. PO2 in mitochondria ≥ 18 mmHg required to generate high energy phosphate bonds e.x ATP PO2 in mitochondria ≥ 18 mmHg required to generate high energy phosphate bonds e.x ATP At rest the average adult male consumes about 225-250 ml of O2/min. At rest the average adult male consumes about 225-250 ml of O2/min. This can increase up to 10 folds during exercise. This can increase up to 10 folds during exercise. There’s very small O2 reserve that can be consumed within 4-6 minutes of cessation of spontaneous ventilation. There’s very small O2 reserve that can be consumed within 4-6 minutes of cessation of spontaneous ventilation.

4. Mechanisms of Hypoxia Aerobic Metabolism requires: O2 Utilization O2 Utilization O2 Delivery O2 Utilization O2 Delivery O2 Utilization O2 Delivery O2 Delivery Shift from aerobic to anaerobic metabolism Increase Lactic acid Increase Lactic acid Progressive Acidosis Cell Death

5. Indication of O2 Therapy Short Term OT Long Term OT

6. Indications of Acute O2 Therapy Accepted Indications: Accepted Indications: –Acute hypoxemia: PaO2< 60 mmHg; SaO2 < 90% –Cardiac and Respiratory arrest. –Hypotension. –Low COP and metabolic acidosis. –Respiratory distress. Questionable Indications: Questionable Indications: –Uncomplicated MI. –Dyspnea without hypoxemia –Sickle cell crisis. –Angina. Fulmer & Snider: Chest 86; 1984

7. Long Term O2 Therapy Rationale of Oxygen Therapy: The combined result from the BMRC & American NOTT studies: “The use of supplemental O2 was associated with enhanced survival and improved neuropsychatric well-being in hypoxic with COPD (15 hours)”

8. Rationale of LTOT Long standing hypoxemia can cause many adverse effects: Long standing hypoxemia can cause many adverse effects: –Pulmonary Hypertension. –Cor Pulmnale. –Reduce exercise tolerance. –Neurosychatric impairement. –Reduce exercise tolerance. –Decreased survival.

9. Indications for Long Term Oxygen Therapy (LTOT): Resting room air: Resting room air: –PaO2: < 55 mmHg –SaO2: < 88% Resting PaO2 = 56-59 or SaO2 <89% in the presence of: Resting PaO2 = 56-59 or SaO2 <89% in the presence of: –CHF or P pulmonale in ECG or evidence of P++ in Echo cardiography.

10. Haemoglobin Molecuole H H Globin H H Globin H H

11. Oxygen Dissociation Curve: O2 Sat. 1009080706050403020 10 20 30 40 50 60 70 80 90 100 mmHG

12. Methods of Oxygen Delivery Low-Flow Systems: Low-Flow Systems: –Nasal Canula –Transtracheal Catheter –Simple Face Mask –Reservoir Mask: Partial Repreathing Partial Repreathing Non-Repreathing Non-Repreathing High Flow Systems: High Flow Systems: –Venturi Mask –Reservoir Nebulizer Blenders.

13. Side Effects of Oxygen Therapy Oxygen Toxicity. Oxygen Toxicity. Oxygen Paradox. Oxygen Paradox. Depression of Respiratory Center. Depression of Respiratory Center. Oxygen Poisoning. Oxygen Poisoning. Complications in newborns. Complications in newborns.

14. Oxygen Toxicity Acute Toxicity: Acute Toxicity: –Tracheobronchitis –ARDS

15. Oxygen Toxicity The potential adverse effects of exposure to increased O2 tensions at 1 atmosphere can be divided into: The potential adverse effects of exposure to increased O2 tensions at 1 atmosphere can be divided into: 1.Alterations of normal physiological functions Extra-pulmonary Extra-pulmonary – ↓ Erythropoiesis – Systemic vasoconstriction clinically insignificant – ↓ COP Pulmonary Pulmonary – ↓Hypoxic ventilatory drive –Pulmonary Vasodilatation → V/Q mismatch → ↑ Dead space ↑ Hypoxia –Absorption atelectasis 2.O2 mediated tissue damadge.

16. Acute Toxicity 100% O 2 for 12-24 hrs: Tracheobronchial irritation: 100% O 2 for 12-24 hrs: Tracheobronchial irritation: –Substernal chest pain. –Dry cough. 100% O 2 >24: ↑FOR > Antioxidant defenses 100% O 2 >24: ↑FOR > Antioxidant defenses → Damage to cell & organelle membrane → Loss of Surfactant → Loss of Surfactant → Altered cell permeability ARDS → Inhibition of cell growth and division → Alteration of Nucleic Acid → Cell death