The document discusses the importance of oxygen therapy, tracing its historical development from its discovery in the 18th century to modern portable oxygen concentrators. It details the physiology of oxygen delivery, types of hypoxia, and various methods for detecting hypoxemia, emphasizing the relationship between oxygen levels in blood and tissue. The session aims to cover indications for oxygen therapy, techniques for administration, and potential complications such as oxygen toxicity.

1. Oxygen Therapy 1
Dr. Kaustubh M. Mohite

2. Oxygen…..
• Its not just gas……. It’s a medicine.
• Atmospheric air contains 20.95% of oxygen.
160 mmHg
104 mmHg in alveoli
90 – 100 mmHg in blood

3. Brief history:
Joseph Priestly, an English chemist who, although
discovered the oxygen molecule in 1772
In 1885, the first ever recorded use of oxygen was documented for a
medical purpose. This medical procedure was to treat a patient with
pneumonia by Dr. George Holtzapple
In 1917, Jon Scott Haldane invented the gas mask to protect
and treat soldiers who had been affected by dangerous chlorine
gasses during the First World War.

4. It wasn’t until the 1950’s that the first form of portable medical oxygen
therapy was invented. This portable oxygen was used strictly in ambulances
and on the scene of medical emergencies.
Finally, you could own your own oxygen therapy unit in your home
Oxygen concentrators began to shrink, due to the demand by younger and
more active oxygen therapy patients who wanted smaller and more mobile
machines
Presently, oxygen concentrators are small enough to fit in a purse, bring bike riding,
or even store under your seat on an airplane! Nowadays, some concentrators can
weigh less than 3 pounds, others have over 10 hours of battery life, and some
home units have an oxygen output upwards of 10,000 ml per minute!

5. 4.
Today’s Agenda….
1. Physiology of Oxygen Delivery
2. Hypoxia and Hypoxemia
3. Types of Hypoxia
4. Detection of Hypoxemia
3.
2.
1.

6. Physiology of Oxygen Delivery
1.

7. 1.
Fundaments of gas transfer:
• Gases moves from areas of high concentration (or pressure) to
areas of lower concentration (or pressure).
• Partial pressure:
Pressure that each gas would produce if it occupied the
container alone.
• Total pressure of the gas mixture is the sum of the partial
pressures of all the individual gases.

8. 1.
The Oxygen cascade

9. 1.
• The decrease in PO2 from air to the mitochondrion is known as
the oxygen cascade.
• It is a normal physiological phenomenon.
• Exaggerated in pathological states:
• Hypoventilation
• Ventilation/ perfusion inequality
• Diffusion abnormality

10. 1. Atmosphere
Alveolus
Blood
Tissue

11. 1.
Atmosphere Alveolus
• Atmospheric pressure: 101 kPa = 760 mmHg
• Oxygen: 21%
• Pressure of Oxygen = 21% of 101 = 21.2 kPa (160 mmHg)
• When we breath in, the air is humidified and warmed by our upper
airway.
• At 37℃, the water vapour in trachea is 6.3 kPa.
• Hence, effective PO2 in trachea:
(101 – 6.3) x 21 / 100 = 19.9 kPa (146 mmHg)

12. As the air reaches alveoli:
19.9 kPa
13.4 kPa
This reduction of PO2 is mainly because of the dilution with CO2
which enters the alveoli from the pulmonary capillaries.
1.

13. PAO2 here is calculated by Alveolar Gas Equation:
1.
RQ = respiratory quotient
i.e. ratio of CO2 production to O2 consumption
value – 0.8

14. Alveolus Blood
• In an ideal situation termed as “Perfect Lung”, the PO2 of pulmonary
venous blood would be equal to the PO2 in the alveolus.
• But this does not happen…..
2 main factors which are responsible for this “Alveolar-Arterial difference”
• Ventilation / Perfusion mismatch (d/t increased dead space or shunt)
• Slow diffusion across the alveolar – capillary membrane
1.

15. Ventilation / perfusion (V/Q) mismatch:
1.

16. Present Concept:
• V & Q are both gravity dependent.
• Both variables increase down the lung.
• Perfusion shows about a 5 fold difference between the top
and bottom of lung.
• Ventilation shows about a 2 fold difference:
• Alveoli are relatively more distended towards the base because of
the negative pressure created by the underlying diaphragm.
1.

17. 1.

18. 1.
Wasted Perfusion
(Shunting of blood)
Wasted Ventilation
(Dead spacing)

19. 1.
Lung pathologies which exacerbates physiological shunt:
• Atelectasis
• Consolidation
• Pulmonary edema
• Small airway obstruction
Lung pathologies increasing physiological deadspace:
• Pulmonary embolism
• Pulmonary vaso-occlusive disease

20. Diffusion:
• Oxygen diffuses from the alveolus to the capillary until the
PaO2 is equal to that in the alveolus.
• Total time when blood flows around the alveoli allowing gas
exchange – 0.75 sec.
• But normally, gas exchange is complete by the time the blood
has passed about one third of the way along the pulmonary
capillary.
• In normal lung, gas exchange takes in 0.25 sec.
1.

21. In normal lung at rest:
1.

22. In normal lung, during exercise:
• There is increase in:
• Cardiac output
• Blood flow around the alveoli
Hence the time for gas exchange is decreased (yet complete)
1.
Maintain the increased oxygen
demands of the body

23. Now consider a diseased lung, with an already compromised
alveolar-capillary membrane……
The time taken for gas to transfer from alveoli to capillary is
prolonged in resting state itself
1.

24. And now when this diseased lung is exposed to exercise or
stressful condition,
1.
Hypoxemia develops
Eg. Alveolar Fibrosis

25. 1.
Fick’s Law
Rate of transfer of a gas through
a sheet of tissue
⍺
Difference in the partial pressures of
the gas on either side of the tissue
Area of tissue
Solubility of the gas
Tissue thickness
1
1
Square root of molecular weight

26. 1.

27. 1.
Hypoxic Pulmonary Vasoconstriction
• Pulmonary blood vessels have a unique property to respond to
hypoxia by vasoconstriction.
• Hence reducing blood flow to the under-ventilated areas.
• Protective mechanism

28. 1.

29. 1.
Oxygen carriage by the blood:
• O2 is carried in 2 forms:
• Combined with hemoglobin (98%)
• Dissolved in plasma (2%)
• 1 gm Hb 1.34ml O2
• 1 litre blood with Hb 15 gm/dl 200 ml O2
• As compare to this, only 3ml O2 is dissolved in each litre of
plasma

30. Oxygen Delivery
Adequacy of oxygen delivery to the tissue depends on 3 factors:
• Hemoglobin concentration
• Cardiac output
• Oxygenation
1.

31. 1.

32. 1. Oxygen delivery (ml O2 / min) =
= Cardiac output (lit / min) x Hb concentration (gm / L) x
1.34 (ml O2 in gm of Hb) x % Saturation
= 5000 x 200 / 1000
= 1000 ml O2 / min

33. Hypoxemia & Hypoxia :
Definitions:
Hypoxemia:
Low levels of oxygen in the blood (low blood oxygen saturation or
content)
Hypoxia:
Inadequate oxygen in tissue for normal cell and organ function.
Hypoxemia leads to Hypoxia (not always)
2.

34. Types of Hypoxia
Hypoxemia is the most common cause of Hypoxia (but not the
only cause)
Hypoxemia without hypoxia:
If the patient compensates for low PAO2 by increasing
oxygen delivery (increasing cardiac output).
Hypoxia without hypoxemia:
If the oxygen delivery to the tissue is impaired or if the
tissue is not able to extract oxygen effectively from blood.
3.

35. Total 5 types of hypoxia :
1. Hypoxic hypoxia
2. Stagnant / Circulatory hypoxia
3. Anemic hypoxia
4. Histotoxic hypoxia
5. Oxygen affinity hypoxia
3.

36. Hypoxic Hypoxia
Also known as:
• Hypoxemic Hypoxia
• Arterial Hypoxia
Results from insufficiency of oxygen available to the lungs or
decreased oxygen tension
3.

37. Characterized by:
• Low Arterial pO2
• Low Arterial O2 content.
• Low arterial % O2 saturation of hemoglobin.
• Low A-V pO2 difference.
3.

38. Mechanisms:
• Decreased PaO2
• V/Q mismatch in the lungs causing a widened A-a gradient.
V/Q mismatch responds to Oxygen therapy.
• Increased pulmonary shunt, i.e. perfusion without gas
exchange. Shunts do not respond to Oxygen therapy.
3.

39. Causes:
Low oxygen tension in inspired air:
• High altitude
• Breathing in closed space
Respiratory disorder with decreased pulmonary ventilation:
• Asthma
• Pneumothorax
• Sleep apnea
• Bulbar poliomyelitis
3.

40. Respiratory disorder associated with inadequate oxygenation of
blood:
• Pneumonia
• Fibrosis
• Emphysema
• Pulmonary hemorrhage
• Bronchiectasis
Cardiac disorders:
• Congestive heart failure
• Low cardiac output
3.

41. Anemic Hypoxia:
Hypoxia in which arterial pO2 is normal but the amount of
hemoglobin available to carry oxygen is reduced
3.

42. Reduced tissue oxygenation as a consequence of low Hb or
Hemoglobin with abnormal oxygen carrying capacity.
Causes:
• Decreased number of RBC’s
• Decreased Hb content in blood
• Formation of altered Hb
• Combination of Hb with gases other than O2 and CO2
3.

43. Stagnant / Circulatory Hypoxia:
Also known as “Ischemic Hypoxia”.
Hypoxia in which the blood flow to the tissues is so low or slow
that adequate oxygen is not delivered to them despite a normal
arterial pO2.
3.

44. Pathophysiology:
• Decreased Cardiac output:
Extremely low cardiac output (cardiogenic shock)
causes a decreased mixed venous oxygen tension that does not
permit complete oxygenation of the blood during pulmonary
gas exchange.
• Increased non-pulmonary shunting:
In certain diseases (cirrhosis), large amounts of
blood flow bypass the entire lungs preventing gas exchange.
3.

45. Causes:
• Congestive cardiac failure
• Hemorrhage
• Surgical stroke
• Vasospasm
• Thrombosis
• Embolism
3.

46. Histotoxic Hypoxia
Inability of the tissues to use oxygen, even in the absence of
hypoxemia.
Cyanide Poisoning:
Cyanide interferes with the aerobic cellular
metabolism by destroying the oxidative enzymes completely
paralyzing the cytochrome oxidase system
3.

47. Oxygen affinity hypoxia:
• Occurs when oxygen dissociation curve shifts to left
3.

48. Increases affinity of Hb to Oxygen.
Decreased oxygen delivery to the tissue
Eg: CO poisoning,
Massive blood transfusion
3.

49. Comparison of types of hypoxias:
Types of
Hypoxia
Arterial
pO2
Hb count Blood
flow to
tissue
Arterial O2
content
Arterial
Hb O2
saturation
A-V PO2
difference
Cyanosis Stimulation
of
peripheral
chemo-
receptors
Hypoxic Normal Normal
+ +
Anemic Normal Normal Normal Absent Absent
Stagnant Normal Normal Normal Normal More than
normal
Absent
+
Histo-toxic Normal Normal Normal Normal Normal Less than
normal
Absent
+
3.

50. Detection of Hypoxemia
Numerous ways to measure whether oxygenation is impaired:
1. Arterial oxygen saturation (SpO2 & SaO2)
2. Arterial oxygen tension (PaO2)
3. A-a oxygen gradient
4. PaO2/FiO2 (P/F ratio)
5. a-A oxygen ratio
6. Oxygenation index
4.

51. Arterial Oxygen saturation:
SaO2 – direct measurement of the percent of oxyhemoglobin in
blood using lab tests on arterial blood.
SpO2 – non-invasive measurement of the percent of saturated
hemoglobin in the capillary bed using pulse-oximetry or
co-oximetry.
SpO2 does not measure the molecules like carboxyHb or
methHb.
4.

52. Oxygen content of arterial blood (CaO2) includes bound and
dissolved oxygen and is calculated as:
CaO2 = (1.34 x Hb concentration x SaO2) + (0.0031 x PaO2)
4.
Oxygen combined with Hb Oxygen dissolved in Plasma

53. Pulse Oximetry:
4.
Works on the principle of spectral analysis for measurement of oxygen saturation, i.e.
detection and quantification of components in solution by their unique light absorption
characteristics.
Light emitting diodes of red and infra-red lights – 660 & 940 nm wavelength

54. • The blood, tissue and bone at the site of application absorb much of the
light.
• Some light passes through the extremity which is sensed by the sensor
on the opposite side.
• By calculating the absorption at the 2 wavelengths, the processor can
compute the proportion of Hb which is oxygenated.
• Oximetry depends on the pulsatile flow and produces a graph of the
quality of flow.
• It measures the functional saturation (saturation of Hb capable of
carrying oxygen).
• It assumes that there are no non-functional Hb in the arterial blood and
measures the O2 saturation as:
% Saturation = HbO2 / HbO2 + Hb
4.

55. Arterial Oxygen tension (PaO2)
• Small amount of oxygen that diffuses from the alveolus into
the plasma.
• Measured by arterial blood gas.
• Normally at room air its value is >80 mmHg.
• Cannot be calculated by non-invasive method.
4.

56. A-a oxygen gradient:
• Alveolar to arterial oxygen gradient.
• It is the difference between the amount of oxygen in the
alveoli and the amount of oxygen in the plasma.
A-a oxygen gradient = PAO2 – PaO2
Alveolar gas equation:
4.

57. Normal A-a gradient varies with age:
A-a gradient = 2.5 + 0.21 x age in years
• A-a gradient increases with higher FiO2.
• With higher FiO2, both PAO2 & PaO2 increase.
• However, PAO2 increases disproportionately causing increase
in the gradient.
4.

58. P/F ratio:
• Most commonly used to measure oxygenation in ventilated
patients.
• Normal value – 300 to 500
• < 300: abnormal gas exchange
• < 200: Acute lung injury
• < 100: ARDS
4.

59. a-A oxygen ratio:
PaO2 / PAO2
It predicts the change in PaO2 that will result when the FiO2 is
changed.
Lower limit of normal: 0.77 – 0.82
Most reliable when FiO2 is less than 55%.
4.

60. Oxygenation Index:
• Used in the recent guidelines to grade the severity of ARDS
OI = (MAP x FiO2 / PaO2 ) x 100
• Normal: < 4
• Mild ARDS: 4 – 8
• Moderate ARDS: 8 – 16
• Severe ARDS: > 16
• Requires ECMO: > 20
4.

61. Tomorrow’s topics….
5. Indications of oxygen therapy
6. Techniques of oxygen administration
(Oxygen delivery devices)
7. Newer modalities
8. Oxygen toxicity
8.
7.
6.
5.

62. Thank You