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.
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
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
21.
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
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
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
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
42.
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
45.
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
48.
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
50.
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.
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.