Oxygentherapy MADE SIMPLE

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DR ABHISHEK PRAKASH
MGM MEDICAL COLLEGE INDORE

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  • Why do you as third years need to know about oxygen therapy? Knowing who is responsible is vital Non prescribers (pt group directives) adrenaline in anaphylaxis
  • Monitoring resps oxygen sats not definitive tool need to be looking at other things acccessory muscles etc
  • Oxygentherapy MADE SIMPLE

    1. 1. Oxygen TherapySpeaker: Dr Abhishek PrakashModerator : Dr Parul Jain
    2. 2. HISTORY 1.Oxygen was discovered by Carl Wilhelm Scheele in Uppsala in 1773 but Priestly is often given priority because his work was published first. 2.Oxygen was also discovered by Priestly in 1774 who first realised its importance as a normal constituent of air and called it Dephlosgisticated Nitrous Acid.. 3.In 1777,Lavoisier named it oxygen. 4.Modern oxygen therapy initiated in 1917 by J.S.Haldane
    3. 3. Oxygen Therapy Partial Pr of O2 in insp. gas (Pi o2)Conc. of O2 (Fi o2) Total Pressure (Orthobaric) (Hyperbaric)
    4. 4. HYPERBARIC OXYGENTHERAPY It works on Henry’s Law which states that amount of gas dissolved in a liquid is directly proportional to its partial pressure. So,the PRESSURE GRADIENT is greatly increased between the arterial and hypoxic tissue and this allows an increasd rate of oxygen transport from blood to cells.Thus,Hyperbaric Oxygen therapy is EFFICIENT AND RAPID method of restoring cellular oxygenation. When a patient is given 100% oxygen under pressure, hemoglobin is saturated, but the blood can be hyperoxygenated by dissolving oxygen within the plasma.
    5. 5. HYPERBARIC PHYSICS ANDPHYSIOLOGY The physics behind hyperbaric oxygen therapy (HBOT) lies within the ideal gas laws. The application of Boyle’s law (p1 v1 = p2 v2) is seen in many aspects of HBOT. This can be useful with embolic phenomena such as decompression sickness (DCS) or arterial gas emboli (AGE). As the pressure is increased, the volume of the concerning bubble decreases. This also becomes important with chamber decompression; if a patient holds her breath, the volume of the gas trapped in the lungs overexpands and causes a pneumothorax. Charles’ law ([p1 v1]/T1 = [p2 v2]/T2) explains the temperature increase when the vessel is pressurized and the decrease in temperature with depressurization. This is important to remember when treating children or patients who are very sick or are intubated. Henry’s law states that the amount of gas dissolved in a liquid is equal to the partial pressure of the gas exerted on the surface of the liquid. By increasing the atmospheric pressure in the chamber, more oxygen can be dissolved into the plasma than would be seen at surface pressure.
    6. 6. Application of HENRY’S LAW inHyperbaric Oxygen therapy0.003ml / 100ml of blood / mm PaO2 In normal state,100 ml of blood will dissolve 0.3 ml of oxygen only as it has a PaO2 of 100 mm of Hg.. 3 SCENARIOS1.Breathing Air (PaO2 100mm Hg)0.3ml / 100ml of blood2.Breathing 100% O2 (PaO2 600mm Hg)1.8ml / 100ml of blood3.Breathing 100% O2 at 3 Atm. Pressure5.4ml / 100ml of blood
    7. 7. HBOT ASHYPEROXYGENATION Most oxygen carried in the blood is bound to hemoglobin, which is 97% saturated at standard pressure. Some oxygen, however, is carried in solution, and this portion is increased under hyperbaric conditions due to Henrys law. Tissues at rest extract 5-6 mL of oxygen per deciliter of blood, assuming normal perfusion. Administering 100% oxygen at normobaric pressure increases the amount of oxygen dissolved in the blood to 1.5 mL/dL; at 3 atmospheres, the dissolved-oxygen content is approximately 6 mL/dL, which is more than enough to meet resting cellular requirements without any contribution from hemoglobin. Because the oxygen is in solution, it can reach areas where red blood cells may not be able to pass and can also provide tissue oxygenation in the setting of impaired hemoglobin concentration or function.
    8. 8. HBOT AND BACTERIALKILLING HBOT increases the generation of oxygen free radicals, which oxidize proteins and membrane lipids, damage DNA, and inhibit bacterial metabolic functions. HBO is particularly effective against anaerobes and facilitates the oxygen-dependent peroxidase system by which leukocytes kill bacteria.
    9. 9. HBOT & VASOCONSTRICTION Hyperoxia in normal tissues causes vasoconstriction, but this is compensated by increased plasma oxygen content(almost 6ml %) and microvascular blood flow. This vasoconstrictive effect does, however, reduce posttraumatic tissue edema, which contributes to the treatment of crush injuries, compartment syndromes, and burns.
    10. 10. MODE OF ADMINISTRATION Oxygen at high pressure can be given from a pressure chamber.The patient then receives oxygen from from an ordinary mask and cylinder.A pressure of 2 atm is generally employed. 2 types of chamber are available: 1.Monoplace/Single Occupant A monoplace chamber compresses one person at a time, usually in a reclining position . The gas used to pressurize the vessel is usually 100% oxygen. Some chambers have masks available to provide an alternate breathing gas (such as air). Employees tend to the patient from outside of the chamber and equipment remains outside the chamber; only certain intravenous lines and ventilation ducts penetrate through the hull. 2.Multiplace HYPERBARIC OXYGEN BED: Rate of compression and decompression is controlled from an adjacent console
    11. 11. OXYGEN TRANSPORTHemoglobin is transported as:1.COMBINATION WITH HEMOGLOBINAbout 98.5% of the oxygen in a healthy human being breathing air at sea level pressure is chemically combined with hemoglobin.2 AS DISSOLVED IN PLASMAAround 1.5% which can be increased by increasing PaO2 by hyperbaric oxygen therapy(HENRY LAW)
    12. 12. Transport Contd.. Hemoglobin in blood leaving the lungs is about 98–99% saturated with oxygen, achieving an oxygen delivery of between 950 - 1150 mL/min[15] to the body. In a healthy adult at rest, oxygen consumption is approximately 200 - 250 mL/min,[15] and deoxygenated blood returning to the lungs is still approximately 75%[16][17] (70 to 78%) [15] saturated. Increased oxygen consumption during sustained exercise reduces the oxygen saturation of venous blood, which can reach less than 15% in a trained athlete; although breathing rate and blood flow increase to compensate, oxygen saturation in arterial blood can drop to 95% or less under these conditions
    13. 13. HEMOGLOBINDISSOCIATION CURVES
    14. 14. Oxygen Flux and Requirements The supply of oxygen is dependent upon the hemoglobin (Hb), O2 saturation % (SaO2) and cardiac output (Q). "Oxygen flux" denotes the total amount of oxygen delivered to the body per minute and is given by the equation:Oxygen flux = 1.34 x Hb in g/dL x (SaO2/100) x (Q in mL/min)/100 = 1000 mL/min
    15. 15. O2 Cascade :The Partial pressure of oxygen drops through various stages from 159 mm of Hg to low levels as 8-10 mm of Hg at mitochondria level…..Air Mitochondri a..If Po2 falls below 1-2 m of Hg at mitochondrial level, AEROBIC METABOLISM stops ..which is known as PASTEUR POINT..
    16. 16. O2 Cascade Atm. Air 159mm Hg (20.95 % of 760) (dry)Humidification6 Vol % (47mm Hg) Lower 149mm Hg Resp. Tract 20.95 % of 713 (760- 47) (moist 37oc)
    17. 17. O2 Cascade Lower 149mm Hg Resp. Tract (20.95 % of 713) (moist 37oc) O2 consumption Alv. ventilation 101mm Hg Alveolar (14 % of 713) or (15 % of air 673) 673 = 760 – 47 – 40 PA O2 = FI O2 (Pb – 47) – PaCo2 x F = PI O2 – PaCo2 R.Q = PI O2 – PaCo2 if breathing 100%
    18. 18. O2 Cascade 101mm Hg Alveolar (14 % of 713) or (15 % of air 673) 673 = 760 – 47 – 40 Venous admixture Arteria l blood 97mm Hg Pa O2 = 100 – 0.3 x age (years) mm Hg A – a = 4 – 25 mmHg
    19. 19. O2 Cascade Arteria Pa O2 = 97mm Hg l blood (Sat. > 95 %) Utilization by tissue Cell Mixed PV O2 = 40mm Hg Mitochondri Venous a PO2 blood Sat. 75% 7 – 37 mmHg Pasteur point – The critical level for aerobic metab. to continue (1 – 2 mmHg PO2 in mitochondria)
    20. 20. INDICATIONS OF OXYGENTHERAPYPULMONARY NON PULMONARY1.Acute Asthma 1.Resuscitation(CPR)2.Acute Exacerbation of 2.Major Trauma COPD-PaO2 ≤ 55mmHg or 3.Major hemorrhage 4.Anaphylaxis SaO2 ≤ 88% 5.Acute Myocardial Infarction3.Continuosly in COPD 6.Active Convulsions patients 7.Hypermetabolic states-4.Breathlessness in setting Thyrotoxicosis,Hyperthermi of END STAGE Cardiac a,Anaemia or respiratory failures 8.ANY ILLNESS CAUSING HYPOXEMIA
    21. 21. HYPOXEMIA Criteria 1. Documented hypoxemia In adults, children, and infants older than 28 days, arterial oxygen tension (PaO2) of < 60 mmHg or arterial oxygen saturation (SaO2) of < 90% in subjects breathing room air or with PaO2 and/or SaO2 below desirable range for specific clinical situation In neonates, PaO2 < 50 mmHg and/or SaO2 < 88% or capillary oxygen tension (PcO2) < 40 mmHg
    22. 22. Hypoxia Vs Hypoxemia Hypoxia-This is inadequate O2 tensions at cellular level and cannot be measured Hypoxemia- This is defined as relative deficiency of O2 in arterial blood.
    23. 23. Types of hypoxia1. Hypoxic hypoxia ( decrease diffusion of O2 across the alveolar-capillary membrane -low inspired FiO2 -V/Q inequalities -increased shunt(eg cardiac anomalies)2. Stagnant hypoxia (decreased cardiac output resulting in increased systemic transit time -Shock -Vasoconstrictio3. Anaemic hypoxia ( decreased O2 carrying capacity in the blood) -Anaemia4. Histotoxic Hypoxia(inability to utilise available oxygen) -cyanide poisoning
    24. 24. Benefit of O2 therapy in HypoxiaHypoxic hypoxia (gas phase) +++Anaemic hypoxia (fluid phase – const.) +Stagnant hypoxia (fluid phase – flow) +Histotoxic hypoxia (tissue phase) -
    25. 25. General Goals/Objectives 1.Correcting Hypoxemia 2.Decreasing Symptoms of Hypoxemia Lessen Dyspnoea/work of breathing Improve Mental function 3.Minimising Cardiopulmonary Workload
    26. 26. Goals CONTD.. 3.Minimising Cardiopulmonary Workload Cardiopulmonary system would compensate for HYPOXEMIA by: -Increasing ventilation to get more oxygen in the lungs and in the blood leading to INCREASED WORK OF BREATHING. -Increasing Cardiac output to get more oxygenated blood to tisses which puts EXTRA LOAD ON HEART,IF DISEASED. -HYPOXIA causes pulmonary vasoconstriction and Pulm hypertension which causes increased workload on right side of heart.
    27. 27. Oxygen therapy To ensure safe and effective treatment remember: Oxygen is a prescription drug. Prescriptions should include –1. Flow rate.2. Delivery system.3. Duration.4. Instructions for monitoring.
    28. 28. Oxygen therapyOxygen delivery methods: All systems require.1. Oxygen supply.2. Flow meter.3. Oxygen tubing.4. Delivery device.5. (Humidifier).
    29. 29. Normal Anatomic No Reservoir capacity systemsSmall (50ml)capacitysystem 100-200 ml 3 Ltr/min Large capacity = 50 ml/Sec System 1l- 2L
    30. 30. Delivery Systems: CONCEPT OF ANATOMICAL RESERVOIR: This is air contained in Oropharynx and Nasopharynx which is about 1/3rdof anatomical dead space or 50 ml.. Low flow systems with no capacity systems-NASAL CATHETERS and NASAL CANNULA use it as a reservoir which empties into lungs with each inspiration even when the mouth is wide open..
    31. 31. Oxygen therapyHumidification Is recommended if more than 4 litres/min is delivered. Helps prevent drying of mucous membranes. Helps prevent the formation of tenacious sputum.
    32. 32. HIGH FLOWCLASSIFICATIONAIR ENTRAINMENTSYSTEMS BLENDING DEVICES 1.AE MASK(VENTURI  1.MANUAL GAS MIXER MASK)  2.OXYGEN BLENDER 2.AE NEBULISERS MECHANICAL VENTILATION using ventilator and ETT is a High Flow System..
    33. 33. NO CAPACITY SYSTEMS NASAL CANNULA/NASAL NASAL CATHETER PRONGS Consists of a soft tube 8-14  2 PRONGS protrude 1 cm FG size with several holes into nares and other end is at its end.. attached to oxygen source Length should be from  FiO2 is more unpredictable angle of mouth to tragus than with nasal catheter. Its inserted through nostrils into oropharynx, just below  Humidification becomes an soft palate.. important part in higher It should be changed to flow rates(>4 L/min).. other nostril every 8-10 hours
    34. 34. NO CAPACITY SYSTEMS NASAL CANNULA/NASAL NASAL CATHETER PRONGSADVANTAGES: ADVANTAGES:Longer the end expiratory pause, Allows continuous flow ofhigher the FiO2 oxygen during routine nursingFiO2 delivered ranges from 25- when patient is eating or oral40% suction is done.Roughly,Fio2 changes by 4% for Can be used when the nasogastricevery L/min change in oxygen tube is occuding one nostril.flow rate DISADVANTAGES:DISADVANTAGE: Higher flow rates (>4L/min) mayCauses greater irritation of nasal dry the nasal mucosa and producemucosa local irritation anddermatitis.So,HUMIDIFICATGastric dilatation with high flows ION of oxygen is essential.
    35. 35. FACE MASKS1.SIMPLE FACEMASKAround 100-200 ml of air gathers in this mask.Air enters through exhalation ports and around face mask.Oxygen Flow rate(L/min) FiO2 5-6 0.40 6-7 0.50 7-8 0.60 It has vents/exhalation ports on the sides for the room air to leak in and thereby diluting the source oxygen. Also allows exhaled Co2 to escape. Used when oxygen delivery is required for short periods<12 hours
    36. 36. Simple Face Mask Thus,simple Face mask delivers the oxygen concentration from 40%-60% at a flow rate of 5L to 8L/min respectively. CAUTION: Due to risk of retaining/rebreathing CO2,we should never apply a simple face mask with a delivery rate of less than 5 L/min.
    37. 37. FACE MASKS 2.PARTIAL REBREATHER MASK Utilises 1litre reservoir bag and mask. Delivers oxygen concentrations of 60-90% at a flow rate of 6L to 8L/min respectively. ONE VALVE 1st third(dead space) is breathed into reservoir bag and rebreathed. air enters throug exhalation ports and around the mask(AS IN SIMPLE FACE MASK).
    38. 38. FACE MASKS Contd.3.NON REBREATHER MASK Utilises ONE WAY VALVES-2 VALVES Between reservoir and bag On one exhalation port.Note that other port is same as in simple face mask... It can deliver highest possible oxygen concentration(95% to 100%) at flow rates of 10 to15L/min,provided leak free system is provided,which is rare.Hence,>70% FiO2 is rare One way valves prevent room and expired air from diluting the oxygen concentration. Reservoir bag must be seen to expand freely.
    39. 39. Non Rebreathing Mask
    40. 40. Variables O2 flow rate Patient factors  Inspiratory flow rate  Expiratory time (active exp. flow + exp. pause) Device factors  Physical volume (capacity)  Vent resistance (tight fit)
    41. 41. High Flow devices Supplies given FiO2@ flows higher than inspiratory demand. These use Air Entrainment(AE) systems or Blenders. AE devices are- 1.AEM(Ventimask) 2.AE Nebuliser(Large volume nebuliser) Peak Inspiratory Flow is 3 times minute ventilation.Since 20L/min is upper limit of minute ventilation,maximum inspiratory flow of 60L/min is possible with these devices..
    42. 42. Bag – Valve – Mask assembly (Ambu Resuscitator) Delivers O2 during BOTH spont. & artf. Vent O2 concentration 30 – 50% (without reservoir)   80 – 100% (with reservoir) To deliver 100% O2  Reservoir – as large as bag vol  O flow rate > minute volume (10 l/m) 2 Drawback – keeps rescuer’s hands engaged
    43. 43. FACE MASKS 4.VENTURI MASK
    44. 44. Venturi prnciple. All high flow systems work on venturi principle.It states that if a gas is passed through a narrow orifice at high pressure,it creates SHEARING FORCES around the orifice which entrain room air in a specific ratio.. Thus,its important that inspiratory gas flows should be 3 to 4 times minute volume. Minute volume is tidal volume times respiratory rate i.e. 500* 12= 6000ml/min.
    45. 45. VENTURI PRINCIPLE
    46. 46. Venturi Mask FLOW RATE DELIVERED O2(FiO2) 02 24% 04 28% 06 31% 08 35% 10 40% 15 60%
    47. 47. BLENDING SYSTEMS These are used when entrainment systems cannot provide high enough FiO2 @ high flows. TYPES 1.Manual gas mixers-Individual oxygen and air flowmeters combined for a desired FiO2 and Flow. 2.Oxygen Blenders.
    48. 48. Air oxygen blender
    49. 49. Incubator Small infants – not on ventilator Works on venturi principle Complete air change – 10 times / hour Control of humidity & temperature O2 conc. falls rapidly when access ports are open
    50. 50. O2 tents For children – not tolerating mask / catheter Large capacity system Upto 50% O2 concentration Large tent cap. and leak port – limited CO 2 build up. Disadvantage  Limited access  Risk of fire  Conflict in O therapy / nursing care 2
    51. 51. Oxygen hood
    52. 52. In-patient oxygen therapy-COPD  The goal is to prevent tissue hypoxia by maintaining arterial oxygen saturation (Sa,O2) at >90%.  Main delivery devices include nasal cannula and Venturi mask.  Alternative delivery devices include non-rebreathing mask, reservoir cannula, nasal cannula or transtracheal catheter.  Arterial blood gases should be monitored for arterial oxygen tension (Pa,O2), arterial carbon dioxide tension (Pa,CO2) and pH.
    53. 53.  Arterial oxygen saturation as measured by pulse oximetry (Sp,O2) should be monitored for trending and adjusting oxygen settings. Prevention of tissue hypoxia supercedes CO2 retention concerns. If CO2 retention occurs, monitor for acidaemia. If acidaemia occurs, consider mechanical ventilation.
    54. 54.  Physiological indications for oxygen include an arterial oxygen tension (Pa,O2) <7.3 kPa (55 mmHg). The therapeutic goal is to maintain Sa,O2 >90% during rest, sleep and exertion. Active patients require portable oxygen. If oxygen was prescribed during an exacerbation, recheck ABGs after 30–90 days. Withdrawal of oxygen because of improved Pa,O2 in patients with a documented need for oxygen may be detrimental. Patient education improves compliance
    55. 55. Long-term oxygen therapy
    56. 56.  Long-term oxygen therapy (LTOT) improves survival, exercise, sleep and cognitive performance. Reversal of hypoxemia supersedes concerns about carbon dioxide (CO2) retention. Arterial blood gas (ABG) is the preferred measure and includes acid-base information. Oxygen sources include gas, liquid and concentrator. Oxygen delivery methods include nasal continuous flow, pulse demand, reservoir cannulae and transtracheal catheter.
    57. 57. Monitoring oxygen therapy Oxygen therapy should be given continuously andshould not be stopped abruptly until the patient hasrecovered, since sudden discontinuation can wash-outsmall body stores of oxygen resulting in fall of alveolaroxygen tension. The dose of oxygen should be calculatedcarefully. Partial pressure of oxygen can be measured inthe arterial blood. Complete saturation of hemoglobin inarterial blood should not be attempted. Arterial PO2 of 60mmHg can provide 90% saturation of arterial blood, but ifacidosis is present, PaO2 more than 80 mmHg is required.In a patient with respiratory failure, anaemia should becorrected for proper oxygen transport to the tissue.
    58. 58. When to stop oxygen therapy Weaning should be considered when the patient becomes comfortable, his underlying disease is stabilized, BP, pulse rate, respiratory rate, skin color, and oxymetry are within normal range. Weaning can be gradually attempted by discontinuing oxygen or lowering its concentration for a fixed period for e.g., 30 min. and reevaluating the clinical parameters and SpO2 periodically. Patients with chronic respiratory disease may require oxygen at lower concentrations for prolonged periods.
    59. 59. Dangers of oxygen therapy:Hypoventilation and Carbon Dioxide Narcosis- the increased PO2 decreased and eliminates the hypoxic drive ( esp. in pt. with chronic CO2 retention as in COPD patients.Such patients have respiratory centre insensitive to rising Pco2 )- Under this circumstances O2 must be given at low concentration <30%Absorption Atelectasis- Nitrogen a relatively insoluble and exists 80% by volume of the alveolar gas.N2 assists in maintaining alveolar stability.O2 therapy replaced N2. Once O2 absorb into the blood the alveolar will collapse esp. in alveolar distal to the obstruction.
    60. 60. Dangers of oxygen therapyDrying and Crusting of secretions in respiratory tract- Oxygen promotes combustion.Fire risk is enormously increased by use of high conc.. Of FiO2.Risk of fire is maximum with oxygen tent…
    61. 61. Pulmonary Oxygen Toxicity(Lorrain-Smith Effect)- The exposure of the high O2 and for prolonged period can lead to damage to alveo-capillary membrane- In general FiO2 > 50% for prolonged period shows increased O2 toxicity- Pulmonary changes mimic ARDS (Exudative changes and proliferative changes.)- Sx –cough, burning discomfort, nausea and vomiting, headache, malaise and etcRetrolental Fibroplasia- Excessive O2 to pre-mature infants may result in constriction of immature retinal vessels, endothelial damage, retinal detachment and possible blindness- Recommended that PO2 be maintained between 60-90 mmHg range in neonate
    62. 62. Dangers of oxygen therapy:Central nervous Toxicity(Paul Bert effect)- Exposure to oxygen at in excess of 1.6 atm may result in convulsion,possibly due to inactivation of sulphhydryl containing enzyme which controls level of GABA.Drying and Crusting of secretions in respiratory tract- Unhumidified oxygen can lead to drying and irritation of nasal mucosa and resp passages.It can lead to respiratory discomfort or even blockage of smaller bronchi by inspissated mucus..

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