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. Oxygen Therapy
Partial Pr of O2 in insp. gas
(Pi o2)
Conc. of O2 (Fi o2) Total Pressure
(Orthobaric) (Hyperbaric)
4. HYPERBARIC OXYGEN
THERAPY
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. HYPERBARIC PHYSICS AND
PHYSIOLOGY
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. Application of HENRY’S LAW in
Hyperbaric Oxygen therapy
0.003ml / 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 SCENARIOS
1.Breathing Air (PaO2 100mm Hg)
0.3ml / 100ml of blood
2.Breathing 100% O2 (PaO2 600mm Hg)
1.8ml / 100ml of blood
3.Breathing 100% O2 at 3 Atm. Pressure
5.4ml / 100ml of blood
8. HBOT AS
HYPEROXYGENATION
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 Henry's 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.
9. HBOT AND BACTERIAL
KILLING
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.
10. 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.
11. 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
13. OXYGEN TRANSPORT
Hemoglobin is transported as:
1.COMBINATION WITH HEMOGLOBIN
About 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 PLASMA
Around 1.5% which can be increased by increasing PaO2 by
hyperbaric oxygen therapy(HENRY LAW)
14. 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
17. 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
18. 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..
19. O2 Cascade
Atm. Air 159mm Hg
(20.95 % of 760)
(dry)
Humidification
6 Vol % (47mm Hg)
Lower 149mm Hg
Resp.
Tract 20.95 % of 713 (760-
47)
(moist
37oc)
20. 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%
21. 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
22. 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)
24. INDICATIONS OF OXYGEN
THERAPY
PULMONARY NON PULMONARY
1.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 Infarction
3.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
25. 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
26. 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.
27. Types of hypoxia
1. 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
-Vasoconstrictio
3. Anaemic hypoxia ( decreased O2 carrying capacity in the
blood)
-Anaemia
4. Histotoxic Hypoxia(inability to utilise available oxygen)
-cyanide poisoning
29. General Goals/Objectives
1.Correcting Hypoxemia
2.Decreasing Symptoms of Hypoxemia
Lessen Dyspnoea/work of breathing
Improve Mental function
3.Minimising Cardiopulmonary Workload
30. 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.
31. 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.
34. Normal Anatomic
No Reservoir
capacity
system
sSmall (50ml)
capacity
system 100-
200 ml
3 Ltr/min
Large
capacity = 50 ml/Sec
System 1l-
2L
35. 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..
36. Oxygen therapy
Humidification
Is recommended if more than 4
litres/min is delivered.
Helps prevent drying of mucous
membranes.
Helps prevent the formation of
tenacious sputum.
37. HIGH FLOW
CLASSIFICATION
AIR ENTRAINMENT
SYSTEMS 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..
38. 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
39. NO CAPACITY SYSTEMS
NASAL CANNULA/NASAL
NASAL CATHETER PRONGS
ADVANTAGES: ADVANTAGES:
Longer the end expiratory pause, Allows continuous flow of
higher the FiO2 oxygen during routine nursing
FiO2 delivered ranges from 25- when patient is eating or oral
40% suction is done.
Roughly,Fio2 changes by 4% for Can be used when the nasogastric
every L/min change in oxygen tube is occuding one nostril.
flow rate DISADVANTAGES:
DISADVANTAGE: Higher flow rates (>4L/min) may
Causes greater irritation of nasal dry the nasal mucosa and produce
mucosa local irritation
anddermatitis.So,HUMIDIFICAT
Gastric dilatation with high flows
ION of oxygen is essential.
42. FACE MASKS
1.SIMPLE FACEMASK
Around 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
43. 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.
44. 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).
45. 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.
50. 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..
51. 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
55. 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.
58. 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.
60. 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
61. 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
64. 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.
65. 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.
66. 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
68. 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.
69. Monitoring oxygen therapy
Oxygen therapy should be given continuously and
should not be stopped abruptly until the patient has
recovered, since sudden discontinuation can wash-out
small body stores of oxygen resulting in fall of alveolar
oxygen tension. The dose of oxygen should be calculated
carefully. Partial pressure of oxygen can be measured in
the arterial blood. Complete saturation of hemoglobin in
arterial blood should not be attempted. Arterial PO2 of 60
mmHg can provide 90% saturation of arterial blood, but if
acidosis is present, PaO2 more than 80 mmHg is required.
In a patient with respiratory failure, anaemia should be
corrected for proper oxygen transport to the tissue.
70. 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.
71. 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.
72. Dangers of oxygen therapy
Drying 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…
73. 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 etc
Retrolental 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
74. 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..
Notes de l'éditeur
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