This document discusses oxygen therapy and oxygen toxicity. It aims to provide guidelines for oxygen therapy including indications, goals, delivery methods and their advantages/disadvantages. Prolonged high concentration oxygen can cause pulmonary toxicity similar to ARDS. The optimal oxygen concentration is the lowest that maintains tissue oxygenation below 60% FIO2 to avoid toxicity. Measures like mechanical ventilation and antioxidants can help prevent toxicity from prolonged high concentration oxygen.

4. HISTORY :

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.

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

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.