Oxygen therapy


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Lecture By Dr.Najah Yussif Almubark
ICU doctor Meeqat General Hospital

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Oxygen therapy

  1. 1. HISTORY :
  2. 2. Aim of oxygen therapy To restore tissue oxygen tension towards normal, a partial pressure of 97 mmHg is required at the cellular mitochondria to maintain metabolism.
  3. 3. Goal of O2 therapy : Pao2 Virtually every patient in ICU receives supplementary o2 , surprisingly there are few guidelines for o2 therapy. American College of Chest Physicians and National Heart Lung and Blood Institute recommendations for instituting oxygen therapy & British thoracic socity. 1. Cardiac and respiratory arrest. 2. Hypoxemia (PaO2<7.8 kPa, SaO2<90%). 3. Hypotension (systolic blood pressure <100 mm Hg). 4. Low cardiac output and metabolic acidosis. (bicarbonate<18 mmol/l). 5. Respiratory distress (respiratory rate >24/min).
  4. 4.  GAS EXCHANGE alveolar Po2 never reach the inspired level because of residual air in alveoli at the end of exhalation. When oxygen tension drops because of disease or pulmonary infiltrates, flow can be maintained by increasing pao2 with oxygen supplement.
  5. 5. O2 160 O2 116CO2 0.3 CO2 32H2O 47 H2 O 47N2 596 N2 565 Dead Space Alveoli O2 100 CO2 40 H2 O 47 N2 573 VEIN ARTERY O2 40 O2 95 CO2 46 CO2 40 H2O 47 H2O 47 N2 573 N2 573 CAPILLARY O2 40 CO2 46 H2O 47 N2 573
  6. 6.  OXYGEN CONTENT = (1.3XHBXSaO2)+(0.003XPaO2)ml/100ml OXYGEN DELIVERY = Q X oxygen content ml/mint.( hemodynamics are very important in respiratory failure) OXYGEN FLUX:O2 available in the body= 5000x19.8 = 990ml/min. 100 normal O2 consumption 250 ml/min Large reserve 740ml/min is available. During exercise COP can increase up to 20L/min, If more than this oxygen debt by anaerobic metabolism.
  7. 7. Alveolar hypoventilation. V/Q mismatch. Venous admixture.
  8. 8.  Hypoxia: Is the O2 deficiency at the tissue level. Hypoxemia: is the O2 deficiency on the blood PaO2 < 60mmHg Cyanosis: is the bluish discoloration of the tissue can be detected when reduced Hb 5g% or more. It is often absent in hypoxemic patient with anaemia and easy detected in polycythemia.
  9. 9.  Hypoxic Hypoxia :- Pa02 ,low as 02 prevented to reach pulmonary capillaries. Causes: a) lung Failure e.g. pulmonary fibrosis, ventilation perfusion mismatch. b) Ventilatory Failure e.g. fatigue, depression of RC e.g. narcotics, Pneumothorax , bronchial obstruction. Anaemic Hypoxia -: Decrease 02 carrying capacity (low Hb).
  10. 10. Cont. Stagnant hypoxia - : * Low COP: Low circulation is a problem in organ such as kidney, heart, during shock. Liver and brain are damage by stagnant hypoxia in CCF. * Shock lung can developed in prolonged circulatory collapse, surfactant production ↓ in un- perfuse area. * Local due to vascular occlusion. Histotoxic hypoxia -:Tissue unable to utilized the normal supplement of 02.e.g. cyanide poisoning, septicemia.
  11. 11. Effect of hypoxia1. Respiratory System :-  Dyspnea is by definition breathing in which the subject is conscious of his shortness of breath.  Hyperpnoea general term for ↑ in rate or dept of breathing.  Tachypnea: rapid shallow breathing Tachypnea is due to reflex stimulation of the respiratory center by chemoreceptors in AO & carotid bodies. Which react to lower O2 tension.
  12. 12. Cont.2. Cardiovascular System:- Coronary, systemic, and cerebral vasodilatation. Pulmonary vasoconstriction. ↑ COP, ↑ HR, and ↑ stroke volume. Arterial pressure ↓ in hypoxia but ↑ if hypercapnia co- exist. In severe hypoxia cardiovascular collapse occurs.
  13. 13. Cont.3. Central Nervous System:- The nervous tissues is more susceptible to hypoxia than any tissue of the body. Blood flow ↑ → cerebral edema. ↑ CSF pressure.  Less hypoxia cause drowsiness, disorientation, Headache. Hypotension greatly magnifies the brain damaging effect of hypoxia.
  14. 14. INDICATION OF 0 2 THERAPYDespite the fact that 0 2 inhalation is a therapeutic intervention designed to correct tissue hypoxia, 0 2 administration seems to be more of a knee jerk response to the presence of life threatening conditions. this is supported by recent survey showing that over 50% of hospitalized patient were
  15. 15. TO WHOM I WILL ORDER 02 SUPPLEMENT:1. Respiratory Failure.2. Acute MI.3. Bronchial Asthma.4. Sickle Cells Crises.5. Carbon Monoxide Poisoning, NRM or HCM.6. Gas Gangrene , NRM or HCM.7. Cluster Headache, NRM or HCM.8. Pre Operative & Post Operative.9. Hyperthermia.
  16. 16. To whom I will order O 21. Respiratory failure a. Hypercapnic Respiratory failure, in this type PaO2 <55mmHg & PaCO2 > 46mmHg Goal of therapy : I. To ↑PaO2 > 60mmHg. II. To Achieved SaO2 88 to 90%. III. To prevent vasoconstrictive effect of pulmonary hypertension and corpulmonal. Therefore low flow therapy must be used. Consequently care should be taken to avoid the administration of excessively rich O2 mixture. Devices used Venturi mask with FIO2 22-28% if Pa02 still < 55 after 30 min administer of progressive increment of inspired O2 is undertaken. Blood gas analysis measurement every 30 min in the first 1 - 3 hour. If Pa02 fail to increase and mental status change, intubation and mechanical ventilation indicated.
  17. 17. Cont.B. Non hypercapnic respiratory failure. Goal ↑PaO2 > 60mmHg. Device use Venturi mask with 50% FIO2 if failed to give saturation 90% and PaO2 >60 this mean the patient had severe cardiogenic, pulmonary edema, ARDS. Then NRM to be used as it give FIO2 90%. CXR must be done and show diffused infiltration so patient must be intubated, MV with PEEP.
  18. 18. Cont2. Continuous O2 Therapy: Significantly prolonged and improved the quality of life in hypoxemic patient with COPD. indicated: Patient with: 1. PaO2 55mmHg: 2. Hb > 55 %. 3. With Peripheral edema. 4. ECG show P Pulmonale.
  19. 19. Bronchial Asthma In ER in acute asthmatic attack High flow 6 to 8 L/min must be give. AIM: to keep SaO2 > 90%. Criteria to admission to ICU according to national protocol for management of asthma 2010:1) PaO2 < 60mmHg.2) PaCO2 > 45 mmHg.3) PEF < 30%. In ICU Venturi mask 50 % used if failed CPAP for 1 hour if no response intubation MV, CXR must be done to clear out pneumothorax.
  20. 20. Oxygen Delivery System High Conc. Mask.Venturi NasalMask Cannula
  21. 21. Oxygen Delivery SystemO2 devices are classified into 2 types:-1. Low Flow System which deliver variable FIO2. e.g. N/C, SFM, PRM, NRM.2. High flow system deliver constant FIO2. e.g. Venturi Mask, CPAP Mask, Face Tent, T-Piece, Ventilator Machine.
  22. 22. Low Flow O2 Delivery System O2 flow L/min Approximate (FIO2) 1 24% 2 28 % 3 32 % 4 36 % 5 40 % 6 44 % 7 48 % 8 52 % 9 56 % 10 60 % FIO2 supplied = O2 inhaled L/min x 4 + 20
  23. 23. Low flow O2 Delivery System Device Advantages Dis-advantagesNasal Capacity 50ml – 1/3 Not give FIO2 > 40%Cannula Anatomic Dead Space . Not use with nasal block Safe, Comfortable or polyp.Simple Face Capacity 100 -200ml Interfere with eating &Mask Give 5-10L/min. drink, discomfort to the patient & impractical for Allow patient to breath air if O2 source fails. long term therapy.Non- Capacity 600 -1L Tight, sealed difficult toRebreathing O2 con 60-90% effective maintain in its positionMask in short term therapy.
  24. 24. Patient with Nasal Cannula with Reservoir bag. Patient on CPAP
  25. 25. High Flow O2 delivery System Device Advantages Dis-advantagesVenturi Accurate concentration of O2 concentrationMask O2 given to patient. altered if not fit. Humidity & aerosol can be Uncomfortable for the added. patient.CPAP Non invasively improved Uncomfortable may arterial oxygenation by ↑ need sedation high FRC. risk for aspiration if patient vomits.Face Tent Administer high humidity. Do not deliver Function as high flow accurate O2 system when attached to concentration Venturi. Used in paediatric & burn patients.
  26. 26. Summary in O2 Delivery System That is Mean:- When High FIO2 required CPAP, IPPV When controlled FIO2required Venturi Mask When low FIO2 required N/C SFM When patient uncooperative Face Tent , IPPV may consider.  Humidification is necessary:  Monitoring by blood gas measurement and pulse Oximeter.
  27. 27. Oxygen Therapy Delivery - Respiratory Medicine - YouTube.flv
  28. 28. Adverse Effect Of High 02 Concentration Effect of inhalation of 100% 02:1. N2 eliminated from lungs within 2 min.2. ↓ reduced HB therefore interfere with C02 transportation.3. ↓ RR secondary to removal of stimulatory effect of chemoreceptor.4. ↓ HR, ↑BP, cerebral & coronary vasoconstriction, but pulmonary vasodilatation.5. Prolonged administration of 02 may interfere with red cell formation.6. Retrolental fibroplesia:  Formation of fibro vascular membrane post. To lenses, in premature babies.7. Fire hazard.
  29. 29. When stopping O2 treatment1. While patient breathing room air PaO2 >65mmHg & SaO2 >90%.2. In patient without arterial hypoxemia but at risk of tissue hypoxia. O2 should be stop when acid base state & clinical assessment of vital organ functions are consistent with resolution of tissue hypoxia.
  30. 30. Titrating Oxygen up and down using the mask escalatorThis table below shows APPROXIMATE conversion values. Venturi 24% (blue) 2-4l/min OR Nasal specs 1L Venturi 28% (white) 4-6 l/min OR Nasal specs 2L Venturi 35% (yellow) 8-10l/min OR Nasal spec 4L Venturi 40% (red)10-12l/min OR Simple face mask 5-6L/min Venturi 60% (green) 15l/min OR Simple face mask 7-10L/min Reservoir mask at 15L oxygen flow If reservoir mask is required, seek senior medical input immediately
  31. 31. Oxygen prescribing Summary- Oxygen is a life saving drug- Oxygen must be prescribed- Doctors will prescribe Target saturation- Prescription will be written on Oxygen section on drug chart- Nurses will choose mask and &/flow rate to achieve Target Saturation- Nurses can titrate Oxygen up & down & record on obs chart- Nurses can wean patients off oxygen- Oxygen must be monitored minimum four hourly- Nurses must sign drug chart every drug round
  32. 32. Pulmonary Oxygen Toxicity :- Inhalation of pure O2 can produce a progressive lung injury similar to ARDS. ARDS is a result of inflammatory cell injury, O2 metabolized play and important rule in the damaging effect of inflammation. In a study done, 10 healthy volunteers inhaled 100% O2 for 6- 12 hours. Results in a tracheobronchitis & a ↓in vital capacity. Acute O2 poisoning manifested with convulsion not occur except with hyperbaric O2. Chronic poisoning may occur with O2 concentration above 60% for prolonged time, may be due to reactivation of surfactant and damage to epithelium.
  33. 33. Oxygen ToxicityII Safe Versus Toxic FIO2:- Observed that O2 inhaled dose not ↓VC if FIO2 < 60%. An FIO2 60% was established as the threshold FIO2 separating safe for toxic level of inhaled oxygen. The consensus is that inhalation of a gas mixture with an FIO2 > 60% for longer than 48 hours is a toxic exposure to inhaled O2. If FIO2 > 60% required for longer than few days other measures should be instituted such as mechanical ventilation & PEEP.
  34. 34. Oxygen ToxicityOptimal FIO2:- The recommendation of a universal FIO 2 threshold separating safe from toxic O2. Inhalation is inappropriate because it neglects the contribution of endogenous antioxidant to the risk of O2 toxicity. If antioxidant become depleted, O2 toxicity occur at FIO2 < 60%. Antioxidant ↓ is more common in patient in ICU with prolonged stay. ▲ The optimal FIO2 for safe O2 inhalation is the lowest tolerable FIO2 below 60%.
  35. 35. Preventive Measures for O2 ToxicityGOALS ACTIONLimit O2 Use supplemental O2 only for:-inhalation  Arterial hypoxemia Indirect evidence of tissue dysoxia. High risk for tissue dysoxia.Limit the  If FIO2 > 60% for 48h, consider mechanicalFIO2 ventilation or PEEP.Support Satisfy the RDA for selenium :-Antioxidant If high risk of O2 toxicity, evaluate selenium & IfProtection vit. E status periodically.
  36. 36. Oxygen prescription chart Model for oxygen section in hospital prescription charts DRUG OXYGEN (Refer To Trust Oxygen Policy) Circle target oxygen saturation 88-92% 94-98% Other___ Starting device/flow rate________ PHAR M PRN / Continuous   Tick if saturation not indicated (Saturation is indicated in almost all cases except for palliative terminal care) SIGNATURE / PRINT NAME DATE ddmm yy* Saturation is indicated in almost all cases except for palliative terminal care
  37. 37. Generally ^_^O2 is a drug. A Dr.’s order is required toinitiate O2 tx except in emergencysituationsOrder should include specific SpO2 orO2 flow rate/ FiO2O2 can be started without an order ifhypoxia is suspected. Dr. must becontacted ASAP
  38. 38. Standard wall set-up for O2 requireshumidification (bubble humidifier/ cold neb)Assess fluid level in humidifier with each RNassessment. Change 3x/week + prnPortable O2 set-up: DO NOT incorporatehumidity (risk of water spilling into deliverydevice)
  39. 39. Monitoring O2 to be treated as a drug so need to ensure the rights: Patient Drug (O2) Route (device) Dose (flow/FiO2) Documentation Reason
  40. 40. Safe Handling of O2Cylinders should be placed in secure holderto prevent tipping/ falling when not in useWhen transporting pt on O2, cylinder mustbe secured in a carrier attached to bed,stretchers , wheelchair or crib
  41. 41. Transporting pts on O2 Ensure adequate O2 supply in tank for anticipated length of time Switch to wall O2 if available at destination and TURN TANK OFF! May need to bring 2 tanks for pt’s requiring high flow Change cylinders at 500 psi
  42. 42. ConclusionOxygen is a life saving treatment. Itis widely used, should be prescribedin written (with the required flowrate, method of delivery), clearly andspecific. Careful monitoring duringOxygen therapy is essential.