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HISTORY :
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.
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).
 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.
O2  160                            O2     116
CO2 0.3                            CO2    32
H2O 47                             H2 O    47
N2 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
  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.
Alveolar hypoventilation.
 V/Q mismatch.
 Venous admixture.
 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.
   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).
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.
Effect of hypoxia
1.   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 chemoreceptor's in AO & carotid
        bodies. Which react to lower O2 tension.
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.
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.
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
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.
To whom I will order O 2
1.   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.
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.
Cont
2. 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.
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.
Oxygen Delivery System



              High Conc. Mask.




Venturi            Nasal

Mask              Cannula
Oxygen Delivery System
O2 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.
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
Low flow O2 Delivery System

  Device           Advantages              Dis-advantages

Nasal        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 to
Rebreathing O2 con 60-90% effective   maintain in its position
Mask        in short term therapy.
Patient with Nasal Cannula
    with Reservoir bag.      Patient on CPAP
High Flow O2 delivery System
  Device            Advantages              Dis-advantages
Venturi     Accurate concentration of  O2 concentration
Mask        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.
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.
Oxygen Therapy Delivery - Respiratory Medicine - YouTube.flv
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.
When stopping O2 treatment
1.   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.
Titrating Oxygen up and down
                        using the mask escalator

This 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
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
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.
Oxygen Toxicity
II 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.
Oxygen Toxicity
Optimal 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%.
Preventive Measures for O2 Toxicity
GOALS                          ACTION
Limit 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 mechanical
FIO2         ventilation or PEEP.

Support     Satisfy the RDA for selenium :-
Antioxidant If high risk of O2 toxicity, evaluate selenium &
             If
Protection  vit. E status periodically.
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
Generally ^_^
O2 is a drug. A Dr.’s order is required to
initiate O2 tx except in emergency
situations
Order should include specific SpO2 or
O2 flow rate/ FiO2
O2 can be started without an order if
hypoxia is suspected. Dr. must be
contacted ASAP
Standard wall set-up for O2 requires
humidification (bubble humidifier/ cold neb)
Assess fluid level in humidifier with each RN
assessment. Change 3x/week + prn
Portable O2 set-up: DO NOT incorporate
humidity (risk of water spilling into delivery
device)
Monitoring
 O2 to be treated as a drug so need to
 ensure the rights:
      Patient
      Drug (O2)
      Route (device)
      Dose (flow/FiO2)
      Documentation
      Reason
Safe Handling of O2

Cylinders should be placed in secure holder
to prevent tipping/ falling when not in use
When transporting pt on O2, cylinder must
be secured in a carrier attached to bed,
stretchers , wheelchair or crib
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
Conclusion
Oxygen is a life saving treatment. It
is widely used, should be prescribed
in written (with the required flow
rate, method of delivery), clearly and
specific. Careful monitoring during
Oxygen therapy is essential.
Oxygen therapy
Oxygen therapy
Oxygen therapy
Oxygen therapy

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Oxygen therapy

  • 1.
  • 2.
  • 3.
  • 5. 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.
  • 6. 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).
  • 7.  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.
  • 8. O2 160 O2 116 CO2 0.3 CO2 32 H2O 47 H2 O 47 N2 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
  • 9.  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.
  • 10. Alveolar hypoventilation. V/Q mismatch. Venous admixture.
  • 11.  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.
  • 12. 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).
  • 13. 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.
  • 14.
  • 15. Effect of hypoxia 1. 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 chemoreceptor's in AO & carotid bodies. Which react to lower O2 tension.
  • 16. 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.
  • 17. 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.
  • 18. 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
  • 19. 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.
  • 20. To whom I will order O 2 1. 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.
  • 21. 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.
  • 22. Cont 2. 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.
  • 23. 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.
  • 24. Oxygen Delivery System High Conc. Mask. Venturi Nasal Mask Cannula
  • 25. Oxygen Delivery System O2 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.
  • 26. 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
  • 27. Low flow O2 Delivery System Device Advantages Dis-advantages Nasal 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 to Rebreathing O2 con 60-90% effective maintain in its position Mask in short term therapy.
  • 28. Patient with Nasal Cannula with Reservoir bag. Patient on CPAP
  • 29.
  • 30. High Flow O2 delivery System Device Advantages Dis-advantages Venturi Accurate concentration of O2 concentration Mask 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.
  • 31. 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.
  • 32. Oxygen Therapy Delivery - Respiratory Medicine - YouTube.flv
  • 33. 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.
  • 34. When stopping O2 treatment 1. 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.
  • 35. Titrating Oxygen up and down using the mask escalator This 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
  • 36. 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
  • 37. 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.
  • 38. Oxygen Toxicity II 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.
  • 39. Oxygen Toxicity Optimal 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%.
  • 40. Preventive Measures for O2 Toxicity GOALS ACTION Limit 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 mechanical FIO2 ventilation or PEEP. Support Satisfy the RDA for selenium :- Antioxidant If high risk of O2 toxicity, evaluate selenium & If Protection vit. E status periodically.
  • 41. 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
  • 42. Generally ^_^ O2 is a drug. A Dr.’s order is required to initiate O2 tx except in emergency situations Order should include specific SpO2 or O2 flow rate/ FiO2 O2 can be started without an order if hypoxia is suspected. Dr. must be contacted ASAP
  • 43. Standard wall set-up for O2 requires humidification (bubble humidifier/ cold neb) Assess fluid level in humidifier with each RN assessment. Change 3x/week + prn Portable O2 set-up: DO NOT incorporate humidity (risk of water spilling into delivery device)
  • 44. Monitoring O2 to be treated as a drug so need to ensure the rights: Patient Drug (O2) Route (device) Dose (flow/FiO2) Documentation Reason
  • 45. Safe Handling of O2 Cylinders should be placed in secure holder to prevent tipping/ falling when not in use When transporting pt on O2, cylinder must be secured in a carrier attached to bed, stretchers , wheelchair or crib
  • 46. 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
  • 47. Conclusion Oxygen is a life saving treatment. It is widely used, should be prescribed in written (with the required flow rate, method of delivery), clearly and specific. Careful monitoring during Oxygen therapy is essential.