2. Historical considerations
Carl Wilhelm Scheele – 1773
Discovered O2
John Pristley – 1774
Was the first to publish
a paper on O2
Antoine Lavoisier – 1777
Coined the term “O2”
3. Oxygen:
Colourless
Odourless
Tasteless
Transparent gas
Slightly heavier than air
Constitues 20-21% of atmospheric air
Essential for life
4. Importance of O2 in cell chemistry
Required in aerobic metabolism for:
1. Production of high energy phosphate compounds
(ATP)
2. Dehydrogenation of flavo proteins
3. Biotransformation of drugs
4. Oxidation of certain other substrates..
5. Definations:
Hypoxia: low level of oxygen at tissue level
Hypoxemia: low levels of oxygen in blood
Partial pressure: the pressure exerted on a surface by
the molecules of individual gases.
The partial pressure of oxygen can be calculated
for a given atmospheric pressure, by multiplying
concentration of a gas by the atmospheric or
barometric pressure.
Eg: 760 mm Hg 21% = 160 mm Hg
6. Oxygen cascade
Oxygen cascade refers to the progressive decrease in
the partial pressure of oxygen from the ambient air
to the cellular level.
PO2 in inspired air 150-160 mm Hg
PO2 in alveolar gas (PAO2) 100- 110 mm Hg
PO2 in arterial blood (PaO2) 98 mm Hg
PO2 in Capillary blood 50-80 mm Hg
PO2 in tissues 30- 50 mm Hg
PO2 in cell mitochondria 10- 20 mmHg
7. Factors affecting oxygenation at various levels in
O2 cascade:
Partial pressure Affected by:
Inspired oxygen
PiO2
Barometric pressure
PB
Oxygen concentration
FiO2
Alveolar gas
PAO2
Oxygen consumption
VO2
Alveolar ventilation
VA
Arterial blood
PaO2
Dead space ventilation
Increased V/Q
Shunt
Decreased V/Q
Cellular PO2 Cardiac output
CO
Hemoglobin
Hb
8. Oxygen therapy
Goals of oxygen therapy:
1. Correcting Hypoxemia
By raising Alveolar & Blood levels of Oxygen
Easiest objective to attain & measure
2. Decreasing symptoms of Hypoxemia
Supplemental O2 can help relieve symptoms of
hypoxia
Lessen dyspnoea/work of breathing
Improve mental function
9. 3. Minimizing Cardiopulmonary workload
Cardiopulmonary system will compensate for
Hypoxemia by:
Increasing ventilation to get more O2 in the lungs & to the
Blood
Increased work of breathing
Increasing Cardiac Output to get more oxygenated blood to
tissues
Hard on the heart, especially if diseased
Hypoxia causes Pulmonary vasoconstritcion &
Pulmonary Hypertension
These cause an increased workload on the right side of heart
Over time the right heart will become more muscular & then
eventually fail (Cor Pulmonale)
10. Supplemental o2 can relieve hypoxemia & relieve
pulmonary vasoconstriction &
Hypertension, reducing right ventricular
workload!!
At our institution, minimal acceptable saturation
for post surgical patients who are cared for in non
critical setup is 92%
11. Assessing the need for oxygen therapy
3 basic ways:
Laboratory measures – invasive or noninvasive
PAO2, PaO2, SaO2, SpO2 monitoring
Clinical Problem or condition
postoperative patients, pneumonia, atelectasis,
pulmonary edema, etc…
Symptoms of hypoxemia
Eg: tachycardia, tachypnoea, hypertension,
cyanosis, dyspnoea, disorientation, clubbing, etc
12. Methods of oxygen administration
Method selection depends upon required
concentration of oxygen.
However, during oxygen therapy the relative dangers
of hypoxia and O2 toxicity should be kept in mind.
Criteria for selecting the method:
1. Patient’s GCS and patient’s comfort
2. Level & range of FiO2 required
3. Extent of humidification required
13. Classification of O2 therapy devices
Oxygen
delivery
systems
Low flow
systems
High flow
systems
14. Low flow O2 delivery system
Flow does not meet inspiratory demand
Oxygen is diluted with air on inspiration
These devices have limited reservoir to store
oxygen and are unable to deliver consistent
inspired oxygen concentrations in settings of
varying respiratory rates & tidal volumes.
17. High flow O2 delivery system:
Supplies given FiO2 at flow rates higher than
inspiratory demand.
They are suitable for delivering consistent and
predictable concentrations of oxygen.
Uses entrainment of air to maintain oxygen supply.
Eg: venturi mask, non rebreathing mask, puritan
face mask.
18. Air Entrainment system
Amount of air entrained varies directly
with:
port size
Velocity
The more air
entrained:
Higher flow
Lower FiO2
21. Indications for O2 therapy:
Arterial PO2 < 60 mmHg or SaO2 < 90%
Cardiac & respiratory arrest
Respiratory failure
Cardiac failure or myocardial infarction
Shock of any cause
Increased metabolic demands (eg. Burns, multiple
injuries, severe sepsis)
Post operative state
Carbon monoxide poisoning.
22. Hypoxia
HYPOXIA: A condition in which the oxygen
available is inadequate at the tissue level
Five types of hypoxia:
Anemic
Hypoxemic
Histotoxic
Circulatory
Hypermetabolic
23. Anemic Hypoxia
Having a decreased carrying capacity for oxygen, the pt
with decreased or abnormal Hb
Anemia
Carbon monoxide poisoning
Methemoglobinemia
Sickle Cell Anemia
Treatment involves blood transfusions, hyperbaric
chamber, bone marrow transplant
24. Hypoxemic Hypoxia
Low PAO2 due to the atmosphere
Hypoventilation – PCO2 is rising
Diffusion Defects
The PaO2 will be lower in all cases, but the PCO2 may or
may not be increased.
Treatment: Compensatory actions to reduce inequalities,
supplemental oxygen
25. Histotoxic Hypoxia
Inability for tissues to utilize oxygen available
Cyanide Poisoning will inhibit cellular metabolism
from occuring; the cells can not process the O2
Treatment: Reversal of poisoning, supplemental
oxygen and/or ventilation
26. Circulatory Hypoxia
A decrease in cardiac output results in a low BP and a
prolonged systemic transit time
The PaO2 can be high, but because of the time it takes
to get to the tissues, the pt is hypoxic
Cardiovascular instability or failure
Shock
Arrhythmias
Treatment include increasing cardiac output with use
of cardiovascular drugs and therapy, supplemental
oxygen
27. Hypermetabolic Hypoxia
In some disease states the body requires a slight
increase in metabolism (i.e. – wound healing
requires 5% increase)
Extensive burns and some cancers will cause large
increases metabolism to the point that supplemental
O2 is required
Treatment: Supplemental O2 or FiO2
28. Approach to selecting appropriate O2 delivery
system:
Purpose (Objective)
Increase FiO2 to correct hypoxemia
minimize symptoms of hypoxemia
Minimize Cardiopulmonary workload
Patient
Cause & severity of hypoxemia
Age
Neuro status/orientation
Airway in place/protected
Regular rate & rhythm (minute Ventilation)
Equipment Performance
The more critical, the greater need for high stable FiO2
Becomes more difficult the more critical due to pt varying pattern
29. Pt Categories
Emergency
Highest FiO2 possible
Highest PaO2 possible
Critical Adult
>60% O2
PaO2 >60mmHg
SpO2 >90%
Stable adult, acute illness, mild hypoxemia
Low to moderate FiO2
Response to therapy, not precise concentrations
30. Chronic dz adult, acute on chronic illness
Ensure adequate oxygenation without depressing
Ventilation
• SpO2 85-90%
• PaO2 50-60mmHg
• Use ventilating mask to control FiO2 precision
31. • Assess response to therapy!!
• If not maintainable on Cannula, use masks
Pt may remove mask frequently due to
• Discomfort
• Convenience
• Change in mental status
Encourage Cannula use between mask use if
mask must come off for periods
32. Precautions & Hazards
O2 Toxicity
Primarily affects Lungs & CNS
2 determining factors of O2 toxicity
PO2
Time of exposure
i.e., higher the PO2 & exposure time the greater the
toxicity.
CNS effects occur with Hyperbaric Pressures
Pulmonary effects can occur @ clinical PO2 levels
Patchy infiltrates on x-ray, prominent in lower lung
fields
Major alveolar injury
33. Pathophysiology
High PO2 damages capillary endothelium
Followed by interstitial edema & AC
membrane thickening
Type I cells are destroyed (cells that create
new lung tissue, gas exchange cells)
Type II cells proliferate (trigger inflamatory
response)
34. Exudative phase
• Alveolar fluid buildup (from inflamatory response)
leads to
low ventilation/perfusion ratio (shunting)
hypoxemia
Hyaline membranes form @ alveolar level
• Proteinaceous eosinophilic (basic) material
• Composed of cellular debris & condensed plasma
proteins.
Pulmonary fibrosis develop
Pulmonary Hypertension develops
35. Treatment:
Try to keep pt alive while reducing FiO2
Cause:
Overproduction of O2 free radicals
• Byproducts of cellular metabolism
• Toxic in excessive amounts
• Normally antioxidants & other special enzymes dispose of excess
free radicals
• Neutrophils (WBC’s) & macrophages flood the infiltrate the tissue
& mediate inflammation response, leading to more free radicals
36. How much is too much?
>50% for very extended times
>PO2 the less time it takes
Goal of ideal oxygen therapy:
Use the lowest FiO2 possible to maintain
adequate tissue oxygenation
37. Other side effects
Growing lungs are more sensitive to O2
Retinopathy of Prematurity (ROP), more later
Bronchopulmonary Dysplasia (BPD), chronic lung
dz, Absorption Atelectasis, Fire hazards, etc
Depression of Ventilation
Hypercarbic drive is blunted
High PCO2 no longer stimulates pt to
increase Ventilation
Suppression of hypoxic drive
The only stimulus left to increase Ventilation
is due to hypoxia
38. When you add to much O2, (remove the hypoxia) you
effectively remove the neurological stimulus to breathe.
(peripheral chemoreceptor’s)
• Hypoventilation occurs
CO2 continues to elevate to sedative levels
• Pt stops breathing until hypoxic again
• If CO2 is too high, they will remain sedated & causes
Cardiopulmonary arrest
• Never withhold O2 therapy from a
Hypoxic pt (PaO2)
39. Take home message!!
Oxygen is a drug, prescribe it as other
drugs, ie, amount, device and time should be
specified.
If patient’s SpO2 is not good with nasal
cannula, consider changing the device instead
of increasing flow rate.
Overzealous use of oxygen is often without
justification & consideration of toxic effects of
oxygen therapy. So think before such
unaccounted for use of oxygen.
