oxygen therapy general principles

1. ‫الرحيم‬ ‫الرمحن‬ ‫اهلل‬ ‫بسم‬

2. Oxygen therapy
Dr. Radhwan H. AL-khashab
consultant anaesthesiologist & intensivist
2021

3. Introduction
In most medical emergencies, oxygen therapy
should be given quickly and in a high concentration
because the avoidance of tissue hypoxia is of
paramount importance.
Oxygen therapy is administered to hypoxaemic
patients to increase alveolar oxygen partial pressure.
The concentration of inspired oxygen administered
depends on the condition being treated.

4. Basic Applied Cardiovascular
Physiology
Monitoring the cardiovascular system plays a key
role in optimizing the balance between oxygen
delivery and oxygen consumption

5. Oxygen delivery can be calculated from the
multiple of cardiac output and arterial oxygen
content.Arterial oxygen content is determined by
arterial oxygen saturation and haemoglobin
concentration.Oxygen consumption is the total
amount of oxygen consumed by the tissues.The
difference between the amount of oxygen carried
to the tissues (arterial oxygen delivery) and the
amount of oxygen returned to the heart (venous
oxygen delivery) indicates the total amount of
oxygen consumed by the tissues.

6. Mixed venous oxygen saturation reflects the
amount of oxygen returning to the pulmonary
capillaries, since it was not used by the tissues to
support metabolic function.The pulmonary artery
is the site where SvO2 values should be measured.
It is important to sample only at this site to allow
for adequate mixing of blood from the superior and
inferior vena cavae and coronary sinus.

7. If the SvO2 is in the normal range (60–80%), then
the clinician may assume that there is adequate
tissue perfusion. If the SvO2 falls below 60%, a
decrease in oxygen delivery and/or an increase in
oxygen consumption has occurred. If the SvO2 is
elevated above 80%, an increase in oxygen supply
and/or a decrease in demand has occurred.

8. An increase in oxygen delivery can be caused by an
increased FiO2 , Hb, or CO.A decrease in oxygen
consumption can be seen in hypothermic states or
in patients who are anaesthetized, mechanically
ventilated or paralysed. In sepsis, oxygen uptake
into the tissues may be decreased

9. Hemoglobin-Bound O2 & oxygen dissolved
 The concentration of hemoglobin-boundO2 (HbO2) is
determined by the variables in
HbO2= 1.34 × Hb × SaO2.
 The concentration of dissolved oxygen in plasma is
determined by the solubility of oxygen in water (plasma)
and the partial pressure of oxygen (PO2) in blood.The
solubility of O2 in water is temperature-dependent
(solubility increases slightly as temperature decreases).
At normal body temperature (37° C), 0.03 mL of O2 will
dissolve in one liter of water when the Po2 is 1 mm Hg .
This is expressed as a solubility coefficient of 0.03
mL/L/mm Hg (or 0.003 mL/100 mL/mm Hg)
Dissolved O2= 0.003 x Po2

10. Arterial O2 Content
 Arterial O2 Content (Cao2 )The concentration of
O2 in arterial blood (Cao2) can be defined by
combining the two Equations by using the So2
and Po2 of arterial blood (Sao2 and Pao2).
CaO2=(1.34xHbxSao2)+(0.003xPa02)

11. Oxygen Delivery (DO2)
Oxygen Delivery (DO2)The oxygen that enters the
bloodstream in the lungs is carried to the vital organs
by the cardiac output.The rate at which this occurs is
called the oxygen delivery (Do2).The Do2 describes
the volume of oxygen (in milliliters) that reaches the
systemic capillaries each minute. It is equivalent to
the product of the O2 content in arterial blood (Cao2)
in mL/L and the cardiac output (Q) in L/min.
DO2= Q x CaO2 x 10
(The multiplier of 10 is used to convert the Cao2 from
mL/dL to mL/L, so the DO2 can be expressed in
mL/min.)

12. Changes in Partial Pressures

13. Indications of oxygen therapy
The clinical indications for oxygen therapy are too
numerous to list but it is useful to consider the
causes of tissue hypoxia.There are four main
classes of tissue hypoxia:
1. Hypoxaemic hypoxia
2.Anaemic hypoxia.
3. Ischaemic hypoxia
4. Cytotoxic hypoxia

14. Types of hypoxia
1. Hypoxaemic hypoxia
Reduced inspired partial pressure of oxygen, e.g.
Changes in altitude .
Hypoventilation, e.g. caused by narcotics & others.
Diffusion impairment, e.g. pulmonary oedema
Ventilation/perfusion mismatch or shunt, e.g.
pulmonary embolus

15. Types of hypoxia
2. Anaemic hypoxia.
3. Ischaemic hypoxia generalized ischaemia caused
by inadequate cardiac output, e.g. hypovolaemia ,
local ischaemia and hypoxia, e.g. cerebral vascular
accident
4. Cytotoxic hypoxia inhibition of the final oxidative
pathway, e.g. cyanide poisoning

16. O2 dissociation curve
The oxygen dissociation curve is a graph that plots the
proportion of haemoglobin in its oxygen-laden
saturated form on the vertical axis against the partial
pressure of oxygen on the horizontal axis.
The oxygen dissociation curve has a sigmoid shape.
There is often a P50 value expressed on the curve, (the
p50 is an important determinant of O2 delivery /
quantifying the hemoglobin's affinity (willingness to
bond) with oxygen) which is the value that tells us the
partial pressure of oxygen at which the red blood cells
are 50% saturated with oxygen. At an oxygen
saturation of 50%, the PaO2 is approximately 25
mmHg

17. O2 dissociation curve

18. Carbon Dioxide
Dissolved
bound to Hgb
HCO3-

19. O2 = bound (sat%) + dissolved(PaO2)
Bound to Hgb
Dissolved

20. Normal Levels of Oxygen in Arterial and
Venous Blood

21. Ventilation-Perfusion ratios
V/Q
In respiratory physiology, the ventilation/perfusion
ratio (V/Q ratio) is a ratio used to assess the
efficiency and adequacy of the matching of two
variables:
V – ventilation – the air that reaches the alveoli
Q – perfusion – the blood that reaches the alveoli via
the capillaries.

23. Normal V/Q Values and V/Q Ratios
 A normal V value is around (minute volume) 4L of
O2/minute.
 A normal Q value is around (perfusion) 5L of
blood/minute.
Therefore the NormalV/Q ratio is 4/5 or 0.8.
 When theV/Q is > 0.8, it means ventilation exceeds
perfusion. Things that may cause this are a blood clot,
heart failure, emphysema, or damage to the pulmonary
capillaries.
 When theV/Q is < 0.8, it means perfusion exceeds
ventilation. Things that may cause this are aspiration,
blockage of bronchi by a foreign object, pneumonia,
severe asthma, pulmonary edema, or COPD.

24. O2 dissociation curve shift
To the Right
1. High temp.
2. Increase CO2.
3. Low PH.
4. Increase 2,3 DPG
(fresh blood)
To the Left
1. Low temp.
2. DecreaseCO2
3. High PH
4. Decrease 2,3 DPG (old
blood)
5. Fetal hemoglobin

25. Methods of O2 therapy

26. Low-Concentration Oxygen
Therapy
Low-concentration or controlled oxygen therapy is
reserved for patients at risk of type 2 (hypercapnic)
respiratory failure who may be harmed by
uncontrolled high concentrations of oxygen. Patients
with severeCOPD, bronchiectasis, cystic fibrosis,
severe kyphoscoliosis or ankylosing spondylitis are
included in this group, as are patients with chronic
musculoskeletal weakness on home ventilation
therapy

27. Each case must be considered in the light of clinical
findings but, as a general rule, oxygen therapy
should be started at 24 or 28% and gradually
titrated against oxygen saturation (SpO2 ) or
preferably arterial oxygen tension.An SpO2 of 88–
92% is often acceptable in these patients and may
avoid pronounced hypercapnia and respiratory
arrest.

28. Oxygen delivery devices
1. Nasal cannulae are well tolerated, and allow the
patient to continue to eat and drink.They do not
increase dead space, and therefore there is no
possibility of rebreathing expired CO2 . At oxygen
flows of 1–2 L/min there is little or no storage of
oxygen in the nasopharynx during the expiratory
pause, and therefore cannulae behave as a no-
capacity variable-performance device. At flows of 2–4
L/min, significant storage of oxygen may occur, and
so a higher concentration of oxygen can be achieved.
High flow rates can damage the nasal mucosa.

29. 2. Semi-rigid plastic facemasks are
examples of variable-performance devices
with a small capacity. A minimum flow rate of
4 L/min is required to flush expired gas from
the mask chamber and thereby prevent
rebreathing of expired CO2 . At higher flow
rates oxygen accumulates within the mask
and enriches the oxygen content of the
subsequent breath.

30. 3. Soft plastic masks with a reservoir bag
have a much larger capacity to store oxygen
during the expiratory pause and can
therefore support higher inspired oxygen
concentrations when used with oxygen flow
rates of 10–15 L/min. If lower flow rates are
used considerable rebreathing of expired gas
accumulating within the large reservoir bag
may occur.

31. 4.TheVenturi mask uses the Bernoulli principle,
described in 1778, in delivering a predetermined
and fixed concentration of oxygen to the patient.
The size of the constriction determines the final
concentration of oxygen for a given gas flow.

33. Oxygen Toxicity
 Oxygen, an element essential to life, may under
certain circumstances produce toxic effects.
 Breathing high concentrations of oxygen at
atmospheric pressure may lead to pulmonary
toxicity. After inspiring 100% oxygen for as little
as 12 h, healthy subjects have reported
retrosternal discomfort, coughing and the urge
to breathe deeply

34.  Tracheobronchitis quickly supervenes and
continued oxygen exposure may lead to
neutrophil recruitment, impairment of surfactant
and acute lung injury (ALI). Exposure to high
concentrations of oxygen for a week may lead to
pulmonary fibrosis.
 Absorption atelectasis.
 Hypoventilation .

35. Retrolental fibroplasia
 Neonates are also thought to be particularly
sensitive to the damaging effects of hyperoxia.
Babies are at risk of developing retrolental
fibroplasias if the eyes are exposed to a PO2 >
10.6 kPa for longer than 3 h while under the age
of 44 post-conceptual weeks.

36. Hyperbaric toxcity
 Hyperbaric conditions may cause pulmonary,
optic and central nervous system toxicity.
Oxygen at 2 bar causes a decrease in vital
capacity of healthy volunteers after only 8 h,
which persists after exposure has ceased.
 Hyperbaric oxygen causes narrowing of the
visual fields and myopia in adults. Eventually,
symptoms and signs of central nervous system
toxicity ensue with nausea, facial twitching,
olfactory/gustatory disturbances and ultimately
tonic-clonic seizures.

37. The End