The document discusses the mechanics of gas exchange and oxygen transportation in the human body, emphasizing the significance of partial pressures, the oxygen cascade, and hemoglobin's oxygen-binding properties. It also covers the clinical aspects of oxygen therapy, including indications, delivery systems, and the importance of individual target saturation levels for different patient populations. It concludes with a warning about the potential toxic effects of prolonged high concentrations of oxygen.

1. DR TARAK NATH CHATTOPADHYAY
MD PGT, MEDICINE, BSMC&H

2.  Total pressure of a gas mixture= σpartial
pressure of invidual gases
 Individual partial pressure α fraction of
volume of that gas

3.  P=760 mm Hg
 components
• O2 20.98%
• N2 78.06%
• Co2 .04%
• Others .92%
 PO2=760× .21=160mm Hg
 PCO2=760× .0004=.3mm Hg

4.  It is the process of decreasing oxygen tension
from atmosphere to mitochondria
 Atmosphere alveoli arterial blood
capillary mitochondria

5.  Water vapour pressure at body temp
=47mmHg
 Thus, Pressure exerted by gas in saturated
moist air = 760-47 = 713mmHg
 Partial pressure of O2 in saturated moist air
= 713 x 0.21 = 149 mmHg
 This is the starting point of O2 cascade.

6.  Down the respiratory tree, O2 tension is
further diluted by the alveolar CO2.
 The partial pressure of alveolar oxygen
(PAO2) is calculated by Alveolar gas equation
PAO2= PiO2-PACO2/RQ
 RQ is the proportion of CO2 produced to the
O2 uptaken
PaCO₂ = PACO₂ ( 40mmHg ) as CO₂ is freely
diffusible.
 PAO2 =149-(40/0.8)~100mmHg

7.  PAO2 100mmHg PcapO2 40mm Hg
 Oxygen diffuses from alveoli to pulmonary
capillaries according to conc gradient
 Oxygenated,blood moves to pulm.
veins→left side of heart→ arterial system
→systemic tissues.

8.  Hb mediated + dissolved state
 O2 carrying capacity of blood= [(1.34 x
HbxSaO2)+(0.003xPaO2)] x Q
 O2 delivery to tissues depends on
1. Hb concentration
2. O2 binding capacity of Hb
3. saturation of Hb
4. amount of dissolved O2
5. cardiac output (Q)

9.  Initially the dissolved O2 is consumed. Then
the sequential unloading of Hb bound O2
occurs.
 PASTEUR POINT is the critical PO2 below
which the O2 delivery is unable to meet the
tissue demands.

12. FACTORS AFFECTING O2
CASCADE AT EACH
LEVEL

13.  High altitude
Patm is less; so does PiO2
 Vapour
URT humidifies inspired air
Increased vapour pressure, decreased PiO2

14.  Amount of CO2 in the alveolus depends on
the metabolism & degree of hypoventilation.
 Fever,sepsis,malignant hyperthermia
increases CO2 production

15.  Ventilation/perfusion mismatch
 • Shunt
 • Slow diffusion

16.  Upperzone overventilated, lower zone
underperfused& underventilated
 Pulmonary venous blood is admixture of all
capillary blood
hence PaO2>PAO2

17.  Deoxygenated blood enters systemic
circulation without getting oxygenated
 Atelectasis, consolidation, small airway
closure

18.  Normal diffusion is rapid.
 Completed by the time blood traverses 1/3
way along pulmonary capillary

19.  PaO2=102-age/3
 Normal Aa gradient 5-15 mHg
 Aa gradient increased in
1. Atelectasis
2. Slowing of diffusion
3. VQ mismatch
4. Mixed venous O2 tension

20.  Serum Hb level.
 Percentage of Hb saturated with O2.
 Cardiac output.
 Amount of dissolved oxygen

22.  Bound to Hb 95%
Dissolved in plasma 5%
 1Hb molecule binds with 4 O2 molecule
 1gm of fully oxygenated Hb contains 1.34ml
of O2 (vary depending on Fe content)
 At an arterial PO2 of 100mmHg,Hb is 98%
saturated,thus 15gm of Hb in 100ml
bloodnwill carry about 20ml of O2 (1.34ml x
15gm x 98/100=20)

23.  Henry’s law :states that the concentration of
any gas in a solution is proportional to its
partial pressure
Gas concentration α partial pressure
 • Dissolved O2 in arterial blood is thus
solubility coefficientx100mmHg
= .003ml/dL×100
=.3 ml

24.  100ml arterial blood carries 20.3 ml O2
 100ml venous blood (PO2 40mm Hg 75%
saturation) contains
1.34x15x75/100=15
 Thus every 100ml of blood passing through
the lungs will take up 5ml of O2

25.  Partial pressure vs
Hb saturation
 It’s a sigmoid
shaped curve with
a steep lower
portion and flat
upper portion
 Describes the
nonlinear
tendency for O2 to
bind to Hb.

26.  One Hb molecule can bind 4 molecules of O2
 Deoxy Hb : globin units are tightly bound in a
tense configuration (T state)
As first molecule of O2 binds, it goes into a
relaxed configuration (R state) thus exposing
more O2 binding sites causing increase in 02
affinity
characteristic sigmoid shape ofODC

27.  The arterial point PO2=100mmHg and
SO2=97.5%
 The mixed venous point PO2=40mmHg and
SO2=75%
 The P50 PO2=27mmHg and SO2=50%

28.  It is the partial pressure at which 50% of Hb
is saturated.
 At a pH of 7.4 , temp 37C , the PO2 at which
the Hb is 50% saturated (P50) is 27mmHg
 When affinity of Hb for 02 is increased , P50
decreases : shift to left in ODC
 When affinity is reduced , P50 increases :
shift to right in ODC

29.  decreased
affinity,increased P50
1. Acidosis
2. Temp
3. 2,3 dpg
4. Pco2
5. Exrcise
anaemia,drugs
(propranolo,digoxi
n)

30.  Decreased P50,
increased affinity
 Alkalosis
 Hypothermia
 Varriant of Hb

31.  Temperature- higher temp, lesser affinity
 Acidosis- deoxyHb has higher affinity to H+
Acute 0.1 pH change causes 3mmHg change
in P50
Chronic depends on body compensatory
mechanism
 CO2
 2,3 DPG

32.  Produced in RBC via EMP shunt in glycolysis
pathway
 Normal level 4 mmol/L
 Binds to deoxyHb-decreases affinity, shift to
right
 Fetal RBC has lower conc of 2,3 DPG thus
higher affinity towards O2

33. INCREASE DECREASE
 Anaemia
 Hypoaxaemia
 Acidosis
 Uraemia
 Liver failure
 Polycytheia
 Hyperoxia
 Alkalosis
 Hypothyroidism

35.  • Hypoxemia : Reduction of oxygen levels in
arterial blood a PaO2 of less than 8.0 kPa
(60 mmHg) or oxygen saturations less than
93%.
 • Hypoxia : Insufficient oxygen supply in the
tissues leads to organ damage

36.  Documented hypoxemia as evidenced by
PaO2 or SaO2 below desirable range for a
specific clinical situation
 Respiratory distress (RR > 24/min)
 Acute care situations in which hypoxemia is
suspected
 Increased metabolic demands (Burns,
multiple injuries, severe sepsis)
 Cardiac failure or myocardial infarction
 Short term therapy (Post anaesthesia
recovery

37.  Correcting Hypoxemia
By raising Alveolar & blood level of oxygen
 Decreasing symptoms of Hypoxemia
Supplemental O2 can relieve symptoms
Lessen dyspnea/ work of breathing
Improve mental function
 Minimizing Cardiopulmonary workload
Cardiopulmonary system will compensate for
hypoxemia by:
• Increase ventilation to get more O2
• Increasing cardiac output to get oxygenated
blood to tissues

38.  •An oxygen delivery system is a device used
to administer, regulate, and supplement
oxygen to a subject to increase the arterial
oxygenation.
 •In general, the system entrails oxygen and
air to prepare a fixed concentration required
for administration.
 Low-flow or variable-performance devices
High-flow or fixed-performance devices.

39.  Provides a fraction of patients minute
ventilation requirement as pure O2. rest of
the ventilatory requirement is fullfilled by
entrailment of room air
 Flow- <6L/min
 Simple, easy to use, well tolerated
 Nasal canula, simple mask, O2 resevoir
canula

40.  Flow 1-6L/in
Fio2 24-44%
 Increasing flow>6L/min
doesnot increases FiO2>44%
 Mucosal drying & damage

41.  Used for moderate flow
over short period of time
 Flow 6-10L/min
FiO2 40-60%
 Holes on each side – air
entrailment &
exhalation
 CO2 can built up inside
mask in flow<6L/min

43.  Function by storing O2 during exhalation
making that that O2 available for next cycle
of inspiration
 Useful for >4L
 Can be moustache/pendent shaped
 Partial rebreather system

44.  They meet patiens inspiratory flow &
generate accurate FiO2
 Flows are such so that air entrailment not
required
 RR & Vt have no affect on FiO2
 Venturi mask, partial/nonrebreather mask,
high flow canula/maskS

46.  Delivers high flow with high conc
 Inhalation & exhalation valve
 Flow10-15l/min
FiO2 60-95%
 Flow rate <6L/min increases chance of
rebreathing CO2

47.  NRB without any valves
 Flow 6-15L/min
FiO2 60-65%
 Patient inhales some of exhaled air
containing CO2

49.  Most often used for critically ill
 Flow 4-12L/min
FiO2 24-60%
 Precise O2 delivery+ minimal chance of CO2
build up- comonly used for COPD
 Holes on each side
colour coded entrailment ports
 Entrailment of room air occurs. Fixed & does
not depend upon PIFR

51. 1 Oxygen is a life saving drug for hypoxaemic
patients.
2 Giving too much oxygen is unnecessary as
oxygen cannot be stored in the body
3 COPD patients (and some other patients) may
be harmed by too much oxygen as this can
lead to increased carbon dioxide (C02) levels
4 Other patients (e.g. myocardial infarction)
may also be harmed by too much oxygen
5 Only give as much as needed– no need for
extra!

52. • Doctors and nurses have a poor
understanding of how oxygen should be used
• Oxygen is often given without a prescription
• If there is a prescription, patients do not
always receive what is specified on the
prescription
• Where there is a prescription with target
range, almost one third of patients are
outside the range

53. • 94-98% Most patients (Those not at risk
of CO2 retention)
• 88-92% C02 retaining patients:
Chronic hypoxic lung disease
COPD
Severe Chronic Asthma
Bronchiectasis / CF
Chest wall disease
Neuromuscular disease
Obesity related hypoventilation
Target saturation should be individualized, should be
reviwed regularly & changed if required.

54. *Saturation is indicated in almost all cases except for
palliative terminal care.

55.  Patients must not go without oxygen while
waiting for medical review a me
 Initial 02 therapy is reservoir mask at 15
litres/minute (RM15)
 Once stable aim for SpO2 94-98% or patient-
specific target range
 COPD patients who are critically ill should
have the same oxygen therapy until blood
gases have been obtained and may then
need controlled oxygen therapy or non-
invasive or invasive ventilation

56.  Record SpO2 before therapy (if possible)
Establish target saturation
 94-98%
Use mask+flow
Repeated BG not necessary if pt within target range
 88-92%
Start with nasal canula 1-2L/min or 28% venturi
Titrate upwards
BG 30-60 min later
 Monitoring
SpO2 5min after any change; record 4hrly
if O2 therapy increases-obtain BG 30-60 min
if O2 therapy dereases- no need for BG

57. Venturi 24% (blue) 2-
3 l/min
OR Nasal cannulae 1L
Venturi 28% (white) 4-
6 l/min
OR Nasal cannulae 2L
Venturi 35% (yellow)
8-12 l/min
OR Nasal cannulae 4L
Venturi 40% (red) 10-
15 l/min
OR Nasal cannulae or Simple face
mask 5-6L/min
Venturi 60% (green)
15 l/min
OR Simple face mask 7-10L/min
Reservoir mask at 15L oxygen flow
If reservoir mask is required, seek senior
medical input immediately

58.  Stop O2 if patient is stable & SpO2 within
normal range on consecutive 2 occassions
 By this time pt is weaned to low dose O2
 Stop supplementary O2 5min- record SpO2
if normal keep pt in room air for 1 hr
weaned if SpO2 normal
 If saturation falls restrat to preivious dose

59.  Harmful effects of breathing molecular O2 at
increased partial pressure
 TIME- MATTERS A LOT !!

60.  Oxygen toxicity – can occur with
 Fio2 > 60% longer than 36 hrs
 Fio2>80%longer than 24 hrs
 Fio2>100%longer than 12hrs

61.  Usually Reactive Oxygen Species (ROS) are
produced during normal physiological
processes like Electron Transport
Chain(ETC),etc.
 The most commonly produced ROS are:
-Superoxide anion (O2
-)
-Hydroxyl radical (OH•)
-Hydrogen peroxide (H2O2)
-Hypochlorous acid (HOCl )

62.  Reactive Oxygen Species (ROS) are a natural
occurrence:
Accidental products of nonenzymatic
and enzymatic processes.
Deliberate production by immune
cells killing pathogens.
UV irradiation, radioactive chemicals, Xrays

63.  Oxygen radicals react with cell
components:
• Lipid peroxidation of membranes.
• Increased permeability → influx Ca2+ →
mitochondrial damage.
• Proteins oxidized and degraded.
• DNA oxidized → breakage.