Oxygen cascade & therapy

An brief illustration of physiological oxygenation Cascade, different oxygenation technique & their appropriate usage

1. Oxygen cascade & therapy DR TARAK NATH CHATTOPADHYAY MD PGT, MEDICINE, BSMC&H

2. DALTON’S LAW Total pressure of a gas mixture= σ partial pressure of invidual gases Individual partial pressure α fraction of volume of that gas

3. Atmospheric air P=760 mm Hg components O2 20.98% N2 78.06% Co2 .04% Others .92% PO2=760× .21=160mm Hg PCO2=760× .0004=.3mm Hg

4. Oxygen cascade It is the process of decreasing oxygen tension from atmosphere to mitochondria Atmosphere alveoli arterial blood capillary mitochondria

5. humidification Water vapour pressure at body temp =47mmHg Thus , Pressure exerted by gas in saturated moist air = 760-47 = 713mmHg Partial pressure of O2 in saturated moist air = 713 x 0.21 = 149 mmHg  This is the starting point of O2 cascade.

6. alveoli Down the respiratory tree, O2 tension is further diluted by the alveolar CO2. The partial pressure of alveolar oxygen (PAO2) is calculated by Alveolar gas equation PAO2 = PiO2-PACO2/RQ RQ is the proportion of CO2 produced to the O2 uptaken PaCO ₂ = PACO₂ ( 40mmHg ) as CO₂ is freely diffusible . PAO2 =149-(40/0.8)~100mmHg

7. Alveoli to blood PAO2 100mmHg PcapO2 40mm Hg Oxygen diffuses from alveoli to pulmonary capillaries according to conc gradient O xygenated,blood moves to pulm . veins →left side of heart→ arterial system →systemic tissues .

8. O2 delivery to tissue Hb mediated + dissolved state O2 carrying capacity of blood= [(1.34 x HbxSaO2)+(0.003xPaO2)] x Q O2 delivery to tissues depends on Hb concentration O2 binding capacity of Hb saturation of Hb amount of dissolved O2 cardiac output (Q)

9. Umloading of O2 at tissues Initially the dissolved O2 is consumed. Then the sequential unloading of Hb bound O2 occurs . PASTEUR POINT is the critical PO2 below which the O2 delivery is unable to meet the tissue demands.

10. O2 cascade

11. FACTORS AFFECTING O2 CASCADE AT EACH LEVEL

12. 1.Atmosphere to alveolus High altitude Patm is less; so does PiO2 Vapour URT humidifies inspired air Increased vapour pressure, decreased PiO2

13. 2.alveoli Amount of CO2 in the alveolus depends on the metabolism & degree of hypoventilation. Fever,sepsis,malignant hyperthermia increases CO2 production

14. 3.Alveoli to capillary Ventilation/perfusion mismatch • Shunt • Slow diffusion

15. Vq mismatch Upperzone overventilated , lower zone underperfused & underventilated Pulmonary venous blood is admixture of all capillary blood hence PaO2>PAO2

16. shunts Deoxygenated blood enters systemic circulation without getting oxygenated Atelectasis , consolidation, small airway closure

17. Diffusion rate Normal diffusion is rapid. Completed by the time blood traverses 1/3 way along pulmonary capillary

18. 4.Alveolo-arterial gradient PaO2=102-age/3 Normal Aa gradient 5-15 mHg Aa gradient increased in Atelectasis Slowing of diffusion VQ mismatch Mixed venous O2 tension

19. 5. Artery to tissue Serum Hb level. Percentage of Hb saturated with O2. Cardiac output. Amount of dissolved oxygen

20. Oxygen dissociation curve

21. Oxygen carriage by blood Bound to Hb 95% Dissolved in plasma 5% 1Hb molecule binds with 4 O2 molecule 1gm of fully oxygenated Hb contains 1.34ml of O2 (vary depending on Fe content) At an arterial PO2 of 100mmHg,Hb is 98% saturated,thus 15gm of Hb in 100ml bloodnwill carry about 20ml of O2 ( 1.34ml x 15gm x 98/100=20 )

22. Dissolved o2 Henry’s law :states that the concentration of any gas in a solution is proportional to its partial pressure Gas concentration α partial pressure • Dissolved O2 in arterial blood is thus solubility coefficientx100mmHg = .003ml/dL×100 =.3 ml

23. 100ml arterial blood carries 20.3 ml O2 100ml venous blood (PO2 40mm Hg 75% saturation) contains 1.34x15x75/100=15 Thus every 100ml of blood passing through the lungs will take up 5ml of O2

24. O2 dissociation curve Partial pressure vs Hb saturation It’s a sigmoid shaped curve with a steep lower portion and flat upper portion Describes the nonlinear tendency for O2 to bind to Hb .

25. Why sigmoid One Hb molecule can bind 4 molecules of O2 Deoxy Hb : globin units are tightly bound in a tense configuration (T state) As first molecule of O2 binds, it goes into a relaxed configuration (R state) thus exposing more O2 binding sites causing increase in 02 affinity characteristic sigmoid shape ofODC

26. Special points in odc The arterial point PO2=100mmHg and SO2=97.5% The mixed venous point PO2=40mmHg and SO2=75% The P50 PO2=27mmHg and SO2=50%

27. P50 It is the partial pressure at which 50% of Hb is saturated . At a pH of 7.4 , temp 37C , the PO2 at which the Hb is 50% saturated (P50) is 27mmHg When affinity of Hb for 02 is increased , P50 decreases : shift to left in ODC When affinity is reduced , P50 increases : shift to right in ODC

28. Right shift decreased affinity,increased P50 Acidosis Temp 2,3 dpg Pco2 Exrcise anaemia,drugs ( propranolo,digoxin )

29. Left shift Decreased P50, increased affinity Alkalosis Hypothermia Varriant of Hb

30. Factors affecting odc Temperature- higher temp, lesser affinity Acidosis- deoxyHb has higher affinity to H+ Acute 0.1 pH change causes 3mmHg change in P50 Chronic depends on body compensatory mechanism CO2 2,3 DPG

31. 2,3 dpg Produced in RBC via EMP shunt in glycolysis pathway Normal level 4 mmol /L Binds to deoxyHb -decreases affinity, shift to right Fetal RBC has lower conc of 2,3 DPG thus higher affinity towards O2

32. 2,3 dpg INCREASE DECREASE Anaemia Hypoaxaemia Acidosis Uraemia Liver failure Polycytheia Hyperoxia Alkalosis Hypothyroidism

33. O2 delivery system

34. Hypoxeamia vs hypoxia • Hypoxemia : Reduction of oxygen levels in arterial blood a PaO2 of less than 8.0 kPa (60 mmHg) or oxygen saturations less than 93%. • Hypoxia : Insufficient oxygen supply in the tissues leads to organ damage

35. Indication of oxygen therapy Documented hypoxemia as evidenced by PaO2 or SaO2 below desirable range for a specific clinical situation Respiratory distress (RR > 24/min) Acute care situations in which hypoxemia is suspected Increased metabolic demands (Burns, multiple injuries, severe sepsis) Cardiac failure or myocardial infarction Short term therapy (Post anaesthesia recovery

36. Goals of oxygen therapy Correcting Hypoxemia By raising Alveolar & blood level of oxygen Decreasing symptoms of Hypoxemia Supplemental O2 can relieve symptoms Lessen dyspnea / work of breathing Improve mental function Minimizing Cardiopulmonary workload Cardiopulmonary system will compensate for hypoxemia by: • Increase ventilation to get more O2 • Increasing cardiac output to get oxygenated blood to tissues

37. O2 delivery system •An oxygen delivery system is a device used to administer , regulate, and supplement oxygen to a subject to increase the arterial oxygenation. •In general, the system entrails oxygen and air to prepare a fixed concentration required for administration . L ow-flow or variable-performance devices H igh-flow or fixed-performance devices .

38. Low flow device Provides a fraction of patients minute ventilation requirement as pure O2. rest of the ventilatory requirement is fullfilled by entrailment of room air Flow- <6L/min Simple, easy to use, well tolerated Nasal canula , simple mask, O2 resevoir canula

39. Nasal canula Flow 1-6L/in Fio2 24-44% Increasing flow>6L/min doesnot increases FiO2>44% Mucosal drying & damage

40. Simple mask Used for moderate flow over short period of time Flow 6-10L/min FiO2 40-60% Holes on each side – air entrailment & exhalation CO2 can built up inside mask in flow<6L/min

41. Resevoir canula

42. Resevoir canula Function by storing O2 during exhalation making that that O2 available for next cycle of inspiration Useful for >4L Can be moustache/pendent shaped Partial rebreather system

43. High flow device They meet patiens inspiratory flow & generate accurate FiO2 Flows are such so that air entrailment not required RR & Vt have no affect on FiO2 Venturi mask, partial/ nonrebreather mask, high flow canula / maskS

44. Non rebreather mask

45. Non rebreather mask Delivers high flow with high conc Inhalation & exhalation valve Flow10-15l/min FiO2 60-95 % Flow rate <6L/min increases chance of rebreathing CO2

46. Partial rebreather mask NRB without any valves Flow 6-15L/min FiO2 60-65% Patient inhales some of exhaled air containing CO2

47. Venturi mask

48. Venturi mask Most often used for critically ill Flow 4-12L/min FiO2 24-60% Precise O2 delivery+ minimal chance of CO2 build up- comonly used for COPD Holes on each side colour coded entrailment ports Entrailment of room air occurs. Fixed & does not depend upon PIFR

49. OXYGEN THERAPY

50. points to consider Oxygen is a life saving drug for hypoxaemic patients. Giving too much oxygen is unnecessary as oxygen cannot be stored in the body COPD patients (and some other patients) may be harmed by too much oxygen as this can lead to increased carbon dioxide (C0 2 ) levels Other patients (e.g. myocardial infarction) may also be harmed by too much oxygen 5 Only give as much as needed– no need for extra!

51. problem Doctors and nurses have a poor understanding of how oxygen should be used Oxygen is often given without a prescription If there is a prescription, patients do not always receive what is specified on the prescription Where there is a prescription with target range, almost one third of patients are outside the range

52. Target saturation 94-98% Most patients (Those not at risk of CO 2 retention) 88-92% C02 retaining patients : Chronic hypoxic lung disease COPD Severe Chronic Asthma Bronchiectasis / CF Chest wall disease N euromuscular disease Obesity related hypoventilation Target saturation should be individualized, should be reviwed regularly & changed if required.

53. Oxygen prescription chart *Saturation is indicated in almost all cases except for palliative terminal care.

54. Oxygen therapy by first responders Patients must not go without oxygen while waiting for medical review a me Initial 0 2 therapy is reservoir mask at 15 litres/minute (RM15) Once stable aim for SpO 2 94-98% or patient-specific target range COPD patients who are critically ill should have the same oxygen therapy until blood gases have been obtained and may then need controlled oxygen therapy or non-invasive or invasive ventilation

55. Starting oxygen therapy Record SpO2 before therapy (if possible) Establish target saturation 94-98% Use mask+flow Repeated BG not necessary if pt within target range 88-92% Start with nasal canula 1-2L/min or 28% venturi Titrate upwards BG 30-60 min later Monitoring SpO2 5min after any change; record 4hrly if O2 therapy increases-obtain BG 30-60 min if O2 therapy dereases - no need for BG

56. Venturi 24% (blue) 2-3 l/min OR Nasal cannulae 1L Venturi 28% (white) 4-6 l/min OR Nasal cannulae 2L Venturi 35% (yellow) 8-12 l/min OR Nasal cannulae 4L Venturi 40% (red) 10-15 l/min OR Nasal cannulae or Simple face mask 5-6L/min Venturi 60% (green) 15 l/min OR Simple face mask 7-10L/min Reservoir mask at 15L oxygen flow If reservoir mask is required, seek senior medical input immediately

57. Stoppage of therapy Stop O2 if patient is stable & SpO2 within normal range on consecutive 2 occassions By this time pt is weaned to low dose O2 Stop supplementary O2 5min- record SpO2 if normal keep pt in room air for 1 hr weaned if SpO2 normal If saturation falls restrat to preivious dose

58. Oxygen toxicity Harmful effects of breathing molecular O2 at increased partial pressure TIME- MATTERS A LOT !!

59. duration Oxygen toxicity – can occur with Fio2 > 60% longer than 36 hrs Fio2>80%longer than 24 hrs Fio2>100%longer than 12hrs

60. mechanism Usually Reactive Oxygen Species (ROS ) are produced during normal physiological processes like Electron Transport Chain(ETC),etc. The most commonly produced ROS are: - Superoxide anion (O 2 - ) -Hydroxyl radical (OH•) -Hydrogen peroxide (H 2 O 2 ) - Hypochlorous acid ( HOCl )

61. mechanism Reactive Oxygen Species (ROS) are a natural occurrence: Accidental products of nonenzymatic and enzymatic processes. Deliberate production by immune cells killing pathogens. UV irradiation, radioactive chemicals, Xrays

62. mechanism Oxygen radicals react with cell components : Lipid peroxidation of membranes. Increased permeability → influx Ca 2+ → mitochondrial damage. Proteins oxidized and degraded. DNA oxidized → breakage.