OXYGEN THERAPY is vast diversified topic. in the slide share, we have tried to compile all detailed information in brief. the slides are well versed and all information have been garnered from verified sources. all recent guidelines, standard textbooks have been referred. COURTESY- DEPARTMENT OF CRITICAL CARE MEDICINE, ABVIMS & DR RML HOSPITAL, NEW DELHI.

1. Oxygen Therapy
By
Dr Ankit Purohit
SR, DNBSS CCM
Moderator
Dr Seema Balkrishna Wasnik
Senior Consultant
Department of Critical Care Medicine
ABVIMS and Dr RML hospital
New Delhi

2. Oxygen
• Eighth element on the periodic table.
• At ambient temperature and pressure (ATP), colourless, odourless,
transparent and tasteless gas with the chemical symbol O2.
• Derived from Greek Word “Oxys” , meaning sharp.
“Oxygen sustains life and supports combustion. While
there are many benefits to oxygen by inhalation, it is not
without hazards and toxic effects. It is therefore
important for persons who are responsible for oxygen
administration to be familiar with its indications for use,
potential hazards and equipment” (Kacmarek,
Stoller & Heuer, 2013).

3. Fast Facts about O2
• Makes up 20.9% of air by volume and 23% air by weight.
• except inert elements can oxidize all other elements.
• Is a non-flammable gas.
• Accelerates combustion.
• At -182.9 C (-300◦ F) oxygen is a pale blue liquid.
• Its critical temperature is -118.4 C (above the critical
temperature oxygen exist as a gas regardless of the pressure).

4. Timeline
• 1771 and 1772- the Swedish
pharmacist Karl Scheele in
experiment discovered gas
augmenting combustion. 1777
findings published.
• Joseph Priestly performed same
experiment in 1774, published in
1775.
• Priestly gave PHLOGISTON
THEORY- fire released combustible
material in air. The
dephlogisticated air was oxygen.
• 1778 Antoine Lavoisier named the
gas oxygene, meaning acid former,.
• 1798 -Thomas Beddoes (father of
respiratory medicine) and James
Watt opened PNEUMATIC institute
and treated COPD Asthma.
• 1885 – George Holtzapple, treated
pneumonia using oxygen.
• 1907 – Arbuthnot Lane devised red
rubber nasal tubing, Haldane
Developed oxygen mask.
• Paul Bert and Adolph Fick
Advanced Understanding of oxygen
physiology, during first world war.
• 1936 – Alvan Barach led to
foundation of long term oxygen
therapy.
• 1950- Coats Pierce Gilson used
oxygen cylinders to deliver oxygen
therapy.

5. Overview of topic
1) Oxygen Transport
2) Indications for Oxygen Therapy , Special considerations.
3) Assessment of oxygen therapy.
4) Oxygen Toxicity.
5) Oxygen delivery at patient interface, Oxygen delivery devices
6) Types of Oxygen Delivery & storage Systems

6. Oxygen Disassociation curve
• Most of oxygen is carried as reversible bind to
hemoglobin. Remaining in dissolved form in
plasma which reflects as PaO2.
• Some of the factors affecting the loading and
unloading of oxygen are:
• Blood pH (Bohr effect)
• Body temperature
• Erythrocyte concentration of certain organic
phosphates (e.g., 2,3diphosphoglycerate)
• Rise in tempertaure,2,3 -DPG, Decrease in pH,
shifts curve to right
• Variation to the structure of the hemoglobin
(Hb) molecules (e.g., sickle cells, methemoglobin
(metHb) and fetal hemoglobin (HbF))
• Chemical combinations of Hb with other
substances (e.g., carbon monoxide)
• 50% SpO2- 26.5 mmHg of PaO2.

7. Madan et al; Correlation between the levels of SpO2 and PaO2, Lung
India. 2017, May.

8. Gas exchange and Oxygen cascade
• At capillary level exchange takes place by
diffusion only.
• Difference between atmospheric oxygen
pressure and arterial pressure acts as driving
force.
• PAo2 – 100 mmHg, PVo2 – 40mmHg,
• Usually there is small difference of 5-10
mmHg between PaO2 and PaO2
• 1) right to left shunt between pulmonary and
cardiac circulation
• 2) regional differences between pulmonary
ventilation and blood flow.
• Neonates have lower PaO2 50-80 mmHg due
to more anatomical and physiological shunts.
Alveolar Air Equation
PAO2 = [(PB-PH2O) * FiO2] - PaCO2 /RQ

9. Ref -Doctor’s Podcast, FRCA

10. Fick’s law of diffusion
• The movement of gas across the alveolar-
capillary membrane is best described by
Fick’s law of diffusion.
• Directly proportional to surface area and
inversely to thickness
• At the tissue level, oxygen diffuses from
the blood (Pcapillaries O2 = 40 mmHg )
across the microvasculature and interstitial
space into the cell (Pintracellular O2=
5mmHg)where cellular respiration take
place.
Fick’s Law of Diffusion
V = A x D (P1 - P2)/T
Where the factors affecting gas exchange are:
V = flow of gas (oxygen)
A = cross sectional area available for diffusion
D = diffusion coefficient
P1 - P2 = the partial pressure gradient
P1 = partial pressure of oxygen in the alveolus
(PAO2)
P2 = partial pressure of oxygen in the blood (PaO2)
T = thickness of the membrane (alveolar-capillary
membrane

11. Ref -Doctor’s Podcast, FRCA

12. Ref -Doctor’s Podcast,
FRCA

13. Ref -Doctor’s Podcast, FRCA

14. Dead Space Physiology
• Dead Space constitute the region with ventilation but no
perfusion.
• It start from nose, pharynx, mouth, down till Terminal
bronchioles.
• It constitute about 150 ml.
• In mechanical ventilated patients, circuits, catheter mount,
masks, T-piece constitute dead space.
• Their volume is measured by simply filling water in them and
measuring its quantity.
• Christian Bhor gave initial equation to calculate dead space.
• Enghoff modified it latter, replacing alveolar CO2 with arterial
CO2.
• Exercise cause progressive decrease in dead space, due to
progressive increase in TV .

15. Robertson et al; Dead Space, Physiology of wasted ventilation,2015, series Physiology
in respiratory medicine.

16. Robertson et al; Dead Space, Physiology of wasted ventilation,2015, series Physiology in
respiratory medicine

17. Physiological shunt
• Occurs due to mixing of deoxygenated blood with oxygenated
blood.
• Perfusion of non or poorly ventilated area leads to
deoxygenated blood to get mixed in cardiac output.
• Physiological shunt - is caused by mixing of blood from
Thebesian veins & bronchial veins in pulmonary veins.
Constitute 2% of whole blood.
• Pathologically – Cyanotic heart diseases, Eisenmenger
syndrome, ARDS, Pulmonary Hypertension.

19. BMJ
1998

21. BMJ 1998

23. Highlights
• Inappropriate dose & failure of monitoring has serious
consequences.
• Adequate ventilation, diffusion & circulation; failure of any of
these leads to tissue hypoxia in 4 minutes.
• Mechanism include 2 main types- arterial hypoxemia & O2 Hb
transport system without arterial hypoxemia.
• PaO2 of 40 mmHg – Hyperventilation due to carotid
Chemoreceptors.
• PaO2 of 30 mmHg – Systemic Hypotension and coma.
• Situation of acute hypoxemia in patients with previous chronic
hypoxemia,PaO2 & PvO2 are unreliable. Assessed in
conjunction with clinical state and ABG.

24. Indications for Oxygen Therapy

26. Chart 1 - Oxygen prescription for acutely hypoxaemic patients in hospital.
B R O'Driscoll et al. Thorax 2017;72:ii1-ii90
Copyright © BMJ Publishing Group Ltd & British Thoracic Society. All rights reserved.

30. Chart 2 - Flow chart for oxygen administration on general wards in hospitals. *For Venturi
masks, the higher flow rate is required if the respiratory rate is >30.
B R O'Driscoll et al. Thorax 2017;72:ii1-ii90
Copyright © BMJ Publishing Group Ltd & British Thoracic Society. All rights reserved.

31. Radiopedia.

32. HIGHLIGHTS
• A1 – aim to achieve near normal oxygen saturation for all
acutely ill patients, except risk of hypercapnic respiratory
failure.
• A2 - 94 -98 % target saturation in the patients.
• A3 – Hypercapnic respiratory failure, 88 – 92% saturation
target.
• A5 – Hypoxemia assessment is done in upright position.
• B2 – oxygen saturation is fifth vital sign.
• B4 – quick and precise medical history, never discontinue
oxygen therapy for room air assessment . Urgent clinical
examination. Measure SpO2 and ABG assessment. Track and
Trigger system. NEWS chart .
• C1 – in shock patients, ABG should always be first sample for
assessment. Earlobe blood gas is also acceptable, but less
accurate.

33. Highlights
• C3 - ABG to be done in – Spo2 < 94% , decrease in Spo2 by 3%
or Breathlessness, drowsiness, risk of hypercapnic oxygen
failure. Any illness requiring ABG.
• D1- breathless patient with SpO2 <85%, start on NRBM @ 15
l/min. Target 94 -98% . Gradually move to simple Oxygen mask
or nasal cannula once target reached. For hypercapnic risk
group 88-92% saturation
• E1 – CPR patients after ROSC, 94-98%, mechanical ventilation.
• E2 – critical ill, trauma NRBM with reservoir @15l/min.94-98%
• E3 – drowning ,94-98%. E4- CO poisoning, 100%

34. Highlights
• F1- Asthma, F2- Pneumonia, F3- Lung cancer, F4 – ILD, F5 –
Pneumothorax, F7 – Pleural effusion, F8 – PE, F9 - cardiogenic
pulmonary edema, F11- Anemia, F12- sickle cell crisis, F13 – MI,F14
– stroke, F15,16 – poisoning, F17 – met and renal disorders; Target
94-98%
• G1 – Hypercapnic respiratory failure – 88-92%. Long term smokers,
old aged should be treated as COPD. SPIROMETRY. Venturi mask at
28%, 2- 6 l/min. ABG on arrival, traiged as very urgent.
• Acute exacerbation hypercapnic failure due to more oxygen,
oxygen is withdrawn gradually or patient land in hypoxemia.
• G2- neurological failure, high risk of death. Mechanical ventilation.
• G6 – NIV for chronic patients with pH <7.35.

35. Highlights
• H- Pregnancy – major trauma, sepsis, acute hypoxemia(CVS) 94 -
98%.
• H5- more then 20weeks pregnant, Left lateral tilt or Manual uterine
displacement, to increase venous flow.
• K- Palliative care- Restricted to patients with SpO2<90%.No role for
monitoring.
• L,M- Heliox and Entonox – upper airway obstruction. No good
evidence for exacerbation of Asthma & COPD. Entonox avoided for
analgesia in patients of Type 2 failure.
• N- CPAP and humidified HFNC – sleep disorders patients planned for
surgery. CPAP with saturation target 88-92%.HFNC as alternative to
NRBM in Respiratory Distress.(COVID)
• P – Tracheostomy, laryngectomy- t piece with high flow O2.

36. Highlights
• Q – humidification – in Acute set ups,Not required for low
flow device. Beneficial for viscous secretions.
• R – Nebulisation –Asthma , done by O2 at Flow rate 6 l/min.
Type 2 Respiratory failure, Done by air jet. If to be done by O2,
Duration limited for to 6 minutes.
• S – Prescription – prescribe the device , route and target range
of saturation on clinical notes and drug chart.
• T- Monitoring and Adjusting – Pulse oximeters, ABG at
designated intervals. Regular charting.

37. LTOT – Long Term Oxygen Therapy
• provision of oxygen therapy for continuous use at home for
patients with chronic hypoxemia (PaO2 at or below 7.3 kPa,
(55mHg).
1) oxygen flow rate must be sufficient to raise the waking
oxygen tension above 8 kPa, (60 mmHg)
2) LTOT is likely to be life long
3) LTOT is usually given for at least 15 hours daily, to include
night time, in view of the presence of worsening arterial
hypoxemia during sleep
Reference – BTS guidelines 2006.

38. Indications
• chronic hypoxaemia-long term oxygen therapy is
indicated for the following conditions with chronic
hypoxaemia:
1) chronic obstructive pulmonary disease
2) severe chronic asthma
3) interstitial lung disease
4) cystic fibrosis
5) bronchiectasis
6) pulmonary vascular disease
7) primary pulmonary hypertension
8) pulmonary malignancy
9) chronic heart failure

39. Indications
PaO2 is consistently at or below 7.3 kPa (55 mmHg), a
period of clinical stability (defined as the absence of
exacerbation of chronic lung disease for the previous
five weeks), patients breathing on room air.
clinically stable PaO2 is between 55 mmHg to 60
mmHg , together with the presence of one of the
following:
• secondary polycythaemia.
• clinical and or echocardiographic evidence of
pulmonary hypertension
LTOT should not be prescribed in patients with chronic
hypoxaemia patients with a PaO2 value above 60
mmHg.

40. Indications
Nocturnal hypoventilation
1) obesity Neuromuscular/spinal/chest wall disease.
2) obstructive sleep apnoea (with CPAP therapy)
Palliative Use
palliation of dyspnoea in malignancy and other causes of
disabling dyspnoea due to terminal disease.

41. Assessment of oxygen concentration: Oximetry
• Oximetry is the measurement of blood hemoglobin (Hb)
saturations using spectrophotometry.
• Trace obtained is Plethysmograph
• Hemoximetry (also called CO-oximetry) – performed in
arterial blood gas analysis.
• Pulse Oximetry - portable, non-invasive monitoring technique

42. Jubran et al; critcal
care.2015. 19-272

44. Oxygen toxicity
• Paul Bert who, in 1878, demonstrated
convulsions in larks( bird) exposed to
15-20 ATA (atmosphere absolute) air.
• In 1899, J Lorraine Smith, while trying
to reproduce 'Bert effect', noticed fatal
pneumonia in rats after 4 days of
exposure to 73% oxygen at 1 ATA.
• ACUTE AND CHRONIC OXYGEN
TOXICITY – in acute short duration,
high concentrations;
• in chronic, long duration and low
concentrations.
• In normal humans the first signs of
toxicity appear after about 10 hours of
oxygen at 1 ATA.
• Oxygen concentration of 100% for 24
to 48 hours can be tolerated.
• Oxygen at 2 ATA produces
characteristic pulmonary signs and
symptoms
• beginning with mild carinal irritation on
deep inspiration 3-6 hours into the
exposure,
• intense carinal irritation an
uncontrolled cough after about 10
hours
• finally chest pain and dyspnoea.
• Symptoms subside 4 hours after
cessation of exposure
Chawala et al, Oxygen toxicity, MJAFI 2001; 57 : 131-133.

45. Signs of toxicity
• CNS TOXICITY (PAUL BERT EFFECT)
• twitching of perioral and small muscles of the hand is a fairly constant feature.
• Facial pallor and 'cogwheel' breathing result of intense peripheral vasoconstriction due
to hyperoxia and diaphragmatic twitching respectively.
• If exposure is continued, vertigo and nausea, followed by altered behaviour, clumsiness,
and finally convulsions result.
• PULMONARY TOXICITY(LORRAINE SMITH EFFECT)
• Symptoms appear after a latent period whose duration decreases with increase in P02.
• In normal humans the first signs of toxicity appear after about 10 hours of oxygen at
1 ATA.
• Clinical features can be divided into three Phases
• (a) Tracheobronchitis (b) ARDS (c) Pulmonary
• interstitial fibrosis.
• Absorption atelectasis due to washout of N2 can lead to collapse of parts of the lung in
the event of air trapping.

46. Oxygen delivery at Patient Interface
• Classification of devices –
• 1) fixed vs variable performance.
• 2) Patient dependent vs patient independent
• 3) Low vs high gas flows.
• Fixed performance Devices –They give fixed Fio2 despite
varying patient parameters.
• Variable performance Devices- Patient dependent, give
variable Fio2 depending on patient parameters.
• When gas flow exceeds patient peak INSPIRATORY flow,
oxygen concentration received is patient independent.
• Low flow devices with tight face or nose fitting mask, deliver
Oxygen concentration patient independent.
Ely J., Clapham M.; Delivering oxygen to patients, BJM nov. 2003

48. Low flow oxygen delivery devices
• provide a variable FiO2 depending
on the patient’s/client’s
inspiratory demands.
• As the inspiratory demands
increase, ambient air is entrained
and the FiO2 is maintained.
• O2 delivered by device is diluted
by inspired air
• Nasal Cannula
• Simple Mask
• Partial Rebreather Mask
• Non-Rebreather Mask
• Transtracheal Catheter
Could a Low Flow Oxygen delivery
devices could still deliver
a high FiO2?
Theoretically, a reservoir mask
set at 10 -15 L/min, could
provide an FiO2 of 1.0 if it fit
properly to a patient’s face
and met the patient’s
inspiratory flow demands on
every breath.

49. Low flow oxygen device performances
Richard D Branson and Jay A Johannigman
Respiratory Care January 2013, 58 (1) 86-97; DOI: https://doi.org/10.4187/respcare.02251

50. Nasal Cannula
• Disposable plastic device with protrusions to be fitted in nose.
• Efficacy from 24% to 45% of oxygen concentration with flows upto 6 litres.
Low flow
24-44 %
1 Lmin=24%
2 Lmin=28%
3 Lmin=32%
4 Lmin=36%
5 Lmin=40%
6 Lmin=44%
ADVANTAGE – Patient can be mobilized. Low cost.
DISADVANTAGE - variable FiO2, variable performance.

51. Facemask
• Hudson Mask – fits over
nose and mouth and
contain hole or expiratory
port.
• Held in place by elastic
strap and has metal piece
over nose to fit.
• FiO2 – 40 to 60 % at flow
rates of 6 to 10 l/min.
• ADVANTAGE – higher
oxygen concentrations.
• DISADVANTAGE –
claustrophobia, feeding
not possible,
• Variable performance.

52. Non re-breather mask
• Consist of mask with
reservoir bag.
• Mask has series of non
rebreathing valves.
Between mask and bag,
and the covers of
exhalation port.
• Connected to oxygen pipe.
• Exhaled air doesnt enter
the bag, exhaled trhough
vlaves in mask.
• FiO2 – 60 – 80% @ O2 flow
of 10 – 15 l/min.
• DISADVANTAGE – risk of
suffocation, if bag deflates
with no air flow.

53. Partial Rebreather mask
• No one way valves
• There is mixing of exhaled
and inhaled air.
• FiO2 0f 80 -90 % @ O2 rate
of 10 -15 l/min.
• Suffocation chances are
minimal.

55. Transtracheal catheter
Its post cricothyrotomy.
Rescue procedure to provide
oxygen in patients
with upper airway obstruction.

56. Oxygen Concentrator
• employ selective removal of nitrogen from room
air to increase the concentration of oxygen in the
delivered gas product.
• electrically powered
• Battery-operated portable oxygen concentrators
• function in continuous flow mode and/or pulse
dose or demand mode.
• to separate and concentrate oxygen from the air,
molecular sieves or semi-permeable membranes
are used.
• Molecular sieves use sodium-aluminium silicate
crystals and employ Pressure Swing Adsorption
(PSA) or Vacuum Pressure Swing Adsorption
(VPSA) technology.
• Semi-permeable membranes are thin plastic
membranes that are selectively permeable to O2
molecules and water vapor.

57. High Flow Oxygen Delivery Devices
• High flow oxygen delivery devices will provide a fixed FiO2
(0.24 - 1.0) regardless of the patient’s inspiratory demands.
• High flow devices are following.
1) Air Entrainment Mask (Venturi);
2) Nasal High Flow Oxygen Therapy;
3) Mechanical Ventilators (invasive )
4) NIV, BiPAP, CPAP/APAP Machines (non invasive)
5) Manual Resuscitation Bags
6) Hyperbaric Oxygen Chambers.

58. Venturi mask
• 40 – 60 % concentration is achieved.
• Fixed delivery of fio2.
• Delivers 24-60% oxygen
• Different colours deliver different rates
• Flow rate: Varies with colour. The
correct flow rate to use with each
colour it is shown on mask, along with
the percentage of oxygen delivered.
• Types:
– BLUE = 2-4L/min = 24% O2
– WHITE = 4-6L/min = 28% O2
– YELLOW = 8-10L/min = 35% O2
– RED = 10-12L/min = 40% O2
– GREEN = 12-15L/min = 60% O2

59. Principle of venturi mask

61. Nasal high flow devices
• alternative to standard high-
flow face mask (HFFM)
oxygen therapy. It provides
delivery of up to 60-70 L/min
of heated and humidified,
blended air and oxygen via
wide-bore nasal cannula.
• It is indicated in patients
experiencing respiratory
distress, high breathing rates.
• Due to high flows(upto 70
l/min), it overcomes high
peak inspiratory rates.
• It is indicated as replacement
of NIV, in many patients and
is recommeneded as bridge
to weaning post extubation.

62. HFN Advantage
• 1) HFNC in comparison to venturi show better results post extubation.
• 2) improve patient discomfort and decrease respiratory rate.
• 3) fewer episode of interface displacement.
• 4) decreased need of NIV and re intubation or intubation than venturi.
• 5) high gas flow generate a Positive airway pressure of 2 – 5 mbar, help to
recruit ateletatic lung.
• 6) NHF decrease dead space- a) increased TV. b) improved inspiratory
aerodynamic.

63. Dr Chris Nickson, Life in the Fastlane.

64. NIV(non invasive ventilation)
• CPAP (continuous positive airways pressure)
– High pressure air/oxygen with a tight-fitting mask
– Positive pressure all the time to help keep airways open (split them)
– Used in acute pulmonary oedema and sleep apnoea
• BiPAP (bilevel positive airways pressure)
– High positive pressure on inspiration and lower positive pressure on expiration
– Used in exacerbations of COPD and ARDS

65. Invasive Ventilation
• Provided by securing airway via devices creating a closed
breathing system.
• Endotracheal tube, Supraglottic airway devices and
Tracheostomy.
• They allow controlled ventilation, Pulmonary toileting.
• ETT, tracheostomy protect airway from aspiration.
• Recruitment and administration of PEEP is possible via ETT.
• Positive airway pressure ventilation is possible with complete
rest to exhausted patient.
• Advent of invasive ventilation changed the course of critically
ill patients.

66. Humidification
• Ideally inspired gas should be
humidified to 37◦ C and 44
cmH2O/L (Wattier &
Ward,2011.)
• Dry medical gas inhalation
can lead to crusting , dryness
of secretions and damage to
mucousa.
• Clinical Signs and Symptoms
of Inadequate Airway
Humidification (Cairo &
Pilbeam, 2004)
• Atelectasis
• Dry, non-productive cough
• Increased airway resistance
• Increased incidence of
infection
• Increased work of breathing
• Substernal pain
• Thick dehydrated secretions

67. Type of humidifiers
• PASSIVE- Heat moist exchangers
(HME filters).
• ACTIVE
• Low Flow Oxygen Humidifiers/
UNheated
• Molecular Humidity - bubble type
humidifiers, bubble-diffuser type
• humidifiers used with nasal
cannula.
• Humidity is not indicated at flows
less than 4 L/min (Cairo & Pilbeam,
2004).
• The use of humidity is not
recommended with reservoir type
masks as condensates may affect
the function of the mask (parts
stick together) .
• High Flow Oxygen
Humidifiers/Heated.
• Molecular Humidity- Passover-
type (+/- wick, +/- heater) (e.g.,
used to humidify tracH mask
systems, incubators).
• Aerosol Humidity air entraining jet
nebulizers (+/- baffles, +/- heaters)

68. Hyperbaric oxygen therapy
• Undersea and Hyperbaric Medical Society (UHMS) is an international, nonprofit
organization, it is primary source of information for diving and hyperbaric oxygen.
• The increased pressure inside the chamber, combined with the delivery of 100%
oxygen (FiO2 = 1.0), drives the diffusion of oxygen into the blood plasma at up to
10 times normal concentration.

69. Physiological effects of hyperbaric oxygen
• Based on DALTON law, BOYLES Law, HENRY’S law
• Normal dissolved oxygen in plasma is 3ml/L
• At 3 atmospheric pressure it plasma dissolved oxygen increase to 60 ml/L;
• At 100% arterial PaO2 reaches 2000 mmHg.
• stimulates the growth of new blood vessels to locations with reduced
circulation, improving blood flow to areas with arterial blockage;
• causes a rebound arterial dilation after HBOT, resulting in an increased
blood vessel diameter greater than when therapy began, improving blood
flow to compromised organs;
• stimulates an adaptive increase in superoxide dismutase (SOD),
• Enhance white blood cell action and potentiating germ-killing antibiotics.

70. Leach et al,Hyperbaric Oxygen therapy; BMJ october1998

71. Indications
1. Air or Gas Embolism
2. Carbon Monoxide
Poisoning
3. Cyanide Poisoning
4. Clostridial Myositis and
Myonecrosis (Gas
Gangrene)
5. Crush Injury,
Compartment Syndrome
and Other Acute Traumatic
6. Ischemias
7. Decompression Sickness
8. Arterial Insufficiencies:
9. Central Retinal Artery
Occlusion
10. Enhancement of Healing
In Selected Problem
Wounds
11. Severe Anemia
12. Intracranial Abscess
13. Necrotizing Soft Tissue
Infections
14. Osteomyelitis (Refractory)
15. Delayed Radiation Injury
(Soft Tissue and Bony
Necrosis)
16. Compromised Grafts and
Flaps
17. Acute Thermal Burn Injury
18. Idiopathic Sudden
Sensorneural Hearing Loss

72. Complications
Barotrauma:
• Ear or sinus trauma
• Tympanic membrane
rupture
• Alveolar over distension
and pneumothorax
• Gas embolism
• Oxygen Toxicity:
Central nervous system
(CNS) toxic reaction (Early
signs twitching, sweating,
pallor and restlessness,
followed by seizures or
convulsions.)
•Pulmonary toxic reaction
Other:
• Fire
• Sudden decompression
• Reversible visual changes
• Claustrophobia
• Decreased Cardiac Output
(Cairo & Pilbeam,2004)

73. Oxygen delivery system
There are three main types of oxygen delivery systems:
• Compressed gas cylinders;
• Liquid oxygen in cryogenic containers;
• Oxygen concentrators for medical use.
Systems are chosen based on size, weight , storage capacity and
cost to company.

74. Compressed gas cylinders
• BODY – Steel carbon fiber cylinder. Marked 3AA
MRI – Aluminium alloy cylinders are used. Marked 3AL or 3ALM.
Have flat concave base and tapered neck with tapered screw for valves.
Color coded – White shoulder, black body.
• VALVE – made of Bronze or brass.
Components – port , stem , seat or diaphragm, nut.
Type – packed and diaphragmatic
• PACKED VALVE –TEFLON covers stem as resilient seal to prevent leak. Direct acting.
Withstand high pressures
• DIAPHRAGMATIC VALVE – metal disk which cylinder and act as diaphragm.
can be opened fully at one half to three turns.
• HANDLE WHEEL - used to open close cylinder.

75. Cylinder sizes

76. Pressure units(Dorsch and Dorsch)

77. Dorsch and Dorsch

78. Valves (Dorsch and
Dorsch)

79. Valve outlet connection(Dorsch and Dorsch)

80. Cylinder weight pressure(Dorsch and Dorsch)

81. Calculating flow rate of cylinder
• the following formula can be used:
• Duration of Flow in minutes =(gauge pressure psi - safe residual pressure psi) x
cylinder factor.
• Flow rate would be in Litres/minute.
• Some examples of cylinder factors for different sized cylinders are:
D cylinder 0.16
E cylinder 0.28
M cylinder 1.56

83. Pin Index system (Dorsch and Dorsch)

84. Safety measures
(Dorsch and Dorsch)

85. Guidelines for safe use

86. Cryogenic containers
• They contain compressed liquid oxygen.
• manufactured by fractional distillation of air at an oxygen manufacturing plant.
• oxygen is stored on site in large cryogenic vessels known as dewars.
• Portable liquid oxygen units offer continuous flow or intermittent flow of oxygen to
the patient/client.
Oxygen Dewar

87. Manifold System

88. Shut off valves in pipelines(Dorsch and Dorsch)

89. DISS(DORSCH AND DORSCH)

90. Pipeline connectors

91. Pressure in pipelines(Dorsch AND Dorsch)

92. THANK YOU