1. Oxygen is transported from the lungs to tissues through a multi-step process involving diffusion, binding to hemoglobin, and active transport via blood circulation. (2) Oxygen diffuses from alveoli into pulmonary capillary blood where it binds to hemoglobin, becoming saturated at 98% in the lungs. (3) Oxygen is then transported to tissues where it dissociates from hemoglobin due to lower oxygen partial pressures, supplying oxygen for cellular respiration through diffusion into tissue fluid and cells.

1. OXYGEN AND
CARBON DIOXIDE
TRANSPORT
Dr. Raju Jadhav
DNB PGT
Dept. Of Anaesthesiology
Medica Superspecialty Hospital

2. OXYGEN(O2)
• Key factor for aerobic metabolism.
• Substrate used by cells in max quantity.
• No storage system in tissues, therefore
continuous supply required.

3. O2 TRANSPORT
• The oxygen transport system comprises the following consecutive
processes:
1. Mass transport by active convection of atmospheric air from the
environment to the pulmonary alveolar spaces, powered by the
contraction/relaxation cycling of the respiratory muscles whose
action is regulated mainly by the medullary and pontine respiratory
centers and peripheral chemoreceptors.
2. Passive diffusion occurs across the alveolo-capillary membrane,
through the plasma and across the erythrocyte membrane finally
binding to hemoglobin (HGb) ‘‘driven’’ by a partial-pressure gradient
for oxygen (pAO2 – paO2).
3. Mass transport by active convection of blood from the alveolar
capillaries and the left heart through the vascular distribution system
to all systemic capillaries,and return to the right heart, powered by
the contraction/relaxation cycling of the myocardium, regulated by
the autonomic nervous system, various hormones,and other local
vascular regulatory functions affecting the distribution of blood flow.

4. OXYGEN TRANSPORT
 Carried in bld in 2 forms:
1.By red blood cells
• Bound to Hb.
• 97-98%.
2.Dissolved O2 in plasma
• Obeys Henry’s Law (“Amount of gas dissolved in a
solution is directly proprtional to its partial pressure”)
PO2 x α = O2 conc in sol
α = Solubility Coefficient (0.003mL/100mL/mmHg at
37C)
• Low capacity to carry O2 i.e <2%.

5. HAEMOGLOBIN
•Iron-Porphyrin compound
• Normal adult = HbA =α2β2
• Hb F= α2γ2
• The γ chains ↑ hb affinity
to O2.
• Each gm of Hb can carry
up to 1.34ml of O2,
theoretically up to
1.39 ml/gm.

6. OXYGEN TRANSPORT
 Oxyhemoglobin Formation:
• Oxygen + Hb  Oxyhemoglobin (Reversible)
• When oxygen binds to haemoglobin, it forms
OXYHAEMOGLOBIN.
• In the lungs where the partial pressure of oxygen is high, the
reaction proceeds to the right forming Oxyhemoglobin.
• In the tissues where the partial pressure of oxygen is low, the
reaction reverses. OxyHb will release oxygen, forming
deoxyhemoglobin.

7. HAEMOGLOBIN
Haemoglobin molecules can
transport up to four O2’s
When 4 O2’s are bound to
haemoglobin, it is 100% saturated,
with fewer O2’s it is partially
saturated.
Oxygen binding occurs in
response to the high PO2 in the
lungs
Co-operative binding:
haemoglobin’s affinity for
O2 increases as its
saturation increases.

8. OXYGEN SATURATION &
CAPACITY
• Ratio of oxygen bound to Hb compared to
total amount that can be bound is Oxygen
Saturation.
• Maximal amount of O2 bound to Hb is
defined as the Oxygen Capacity.

9. • O2 CONTENT -The sum of O2 carried on Hb
and dissolved in plasma.
• CaO2 (ml/dL) = (SaO2 x Hb x 1.34) + (PO2 x0.003)
• O2 content in 100 ml blood (in normal adult
with Hb 15 gm/dl) ~ 20 ml/dl
• (19.4 ml as OxyHb + 0.3 ml in plasma)
ARTERIAL O2 CONTENT

10. Venous O2 content (CvO2)
• CvO2 =(SvO2 x Hb x 1.34) + (PvO2 x 0.003)
• Normally-15ml/dl.
• Mixed venous saturation (SvO2 ) measured in
the Pul Artery represents the pooled venous
saturation from all organs.
• SvO2 influenced by changes in both DO2 and
VO2
• Normally, the SvO2 is about 75%, however,
clinically an SvO2 of about 65% is acceptable.

11. TOTAL O2 DELIVERY
• DO2 (ml/min) = Q x CaO2 x 10
• DO2 = Q x Hb x SaO2 x 1.34 x 10
• Q=Cardiac Output and multiplier of 10 is
used to convert CaO2 from ml/dl to ml/L)
• N 900-1,100 ml/min
• Decreased oxygen delivery occurs when
there is:
• ↓ed cardiac output
• ↓ed hemoglobin concentration
• ↓ed blood oxygenation

12. O2 CONSUMPTION
• The amount of oxygen extracted by the peripheral
tissues during the period of one minute is called
oxygen consumption or VO2.
• (N- 200-300ml/min)
• VO2 = Q x (CaO2 - CvO2) x 10
• VO2 = Q x 1.34 x Hb x (SaO2-SvO2) x 10
• O2 consumption is commonly indexed by the
patients body surface area (BSA) and calculated
by:
• VO2 / BSA
• Normal VO2 index is between 110-160ml/min/m2.

13. OXYGEN EXTRACTION RATIO
• The oxygen extraction ratio (O2ER) is the
amount of oxygen extracted by the peripheral
tissues divided by the amount of O2 delivered to
the peripheral cells.
• Also known As: Oxygen coefficient ratio &
Oxygen utilization ratio.
• Index of efficiency of O2 transport .
• O2ER = VO2 / DO2
• Normally ~ 25% but increases to 70-80% during
maximal exercise in well trained athletes

14. FACTORS THAT AFFECT
O2ER
Increased with:
•Decreased CO
•Increased VO2
•Exercise
•Seizures
•Shivering
•Hyperthermia
•Anemia
•Low PaO2
Decreased with:
•Increased Cardiac Output
•Skeletal Muscle Relaxation
•Peripheral Shunting
•Certain Poisons
•Hypothermia
•Increased Hemoglobin
•Increased PaO2

15. A reduction below point 'c' in figure cannot
be
compensated for by an increased oxygen
extraction and
results in anaerobic metabolism and lactic
acidosis.
•In general, DO2 >>VO2.
•When oxygen
consumption is high
(exercise) the ↑ed O2
requirement is usually
provided by an ↑ed CO.
•Alternatively, if oxygen
delivery falls relative to
oxygen consumption the
tissues extract more
oxygen from the Hb (the
saturation of mixed
venous blood falls
below 70%) (a-b )

16. O2 DELIVERY DURING EXERCISE
• During strenuous exercise VO2 may increase to 20 times
Normal
• Blood also remains in the capillary for <1/2 Normal time due
to increased C.O.
• O2 Sat not affected as blood is fully saturated in first 1/3 of
Normal time available to pass through pulmonary circulation.
• Diffusion capacity increases upto 3 fold since:
1. Additional capillaries open up .So increase in no of
capillaries participating in diffusion process.
2. Dilatation of both alveoli and capillaries causing decrease in
alveolo capillary distance.
3. Improved V/Q ratio in upper part of lungs due to increase
blood flow to upper part of lungs.

17. THE EFFECTS OF ANAESTHESIA
• The normal protective response to hypoxia is reduced by
anaesthetic drugs and this effect extends into the post-
operative period.
 Following induction of anaesthesia :
• FRC ↓
• V/Q mismatch is ↑ed
• Atelectasis develops rapidly
• This 'venous admixture' increases from N 1% to around 10%
following induction of anaesthesia.
• Volatile anaesthetic agents suppress hypoxic pulmonary
vasoconstriction.
• Many anaesthetic agents depress CO and therefore ↓ O2 delivery.
• Anaesthesia causes a 15% ↓ in metabolic rate and therefore a
reduction in oxygen requirements.
• Artificial ventilation causes a further 6% ↓ in oxygen requirements as
the work of breathing is removed.

18. OXYGEN CASCADE

19. KEY STEPS IN OXYGEN CASCADE
• Uptake in the lungs
• Carrying capacity of blood
• Delivery to capillaries
• Delivery to interstitium
• Delivery to individual cells
• Cellular use of oxygen

20. UPTAKE IN THE LUNGS FROM ATMOSPHERE
• PO2 = FiO2 * Barometric Pressure.
• So with FiO2 of 21% , PO2 in the atmospheric air is 160mmHg.
• pAO2 = FiO2 * (PB-PH20) – PaC02/R.Q
• The Alveolar Air Equation,represents the partial pressure of oxygen
in alveolar air at the prevailing barometric pressure after accounting
for the vapor pressure of water with which tracheal air becomes
saturated at body temperature.
• It defines the oxygen partial pressure in the steady state accounting
for oxygen extracted and CO2 added by the respiratory gas
exchange. This is the oxygen partial pressure with which blood in
the pulmonary capillaries equilibrates during its rapid transit through
the capillary.
• Approximate normal value of pAO2 is 104 mm Hg.

21. • The Fick equation of diffusion of a gas in a liquid
medium describes the determinants of the
oxygen flux as V = A * D * P1-P2/d
where,
• A is the area available for diffusion;
• D is the diffusion constant for the gas( D= 1 for
O2 and D = 20 for CO2) ;
• P1-P2 is the gas partial pressure difference;
• d is the diffusion distance,
• Thus DP/d is the partial pressure gradient.
• Normal O2 diffusion capacity at alveolo-capillary
membrane is 25 ml/min/mmHg.
GAS DIFFUSION PRINCIPLE

22. UPTAKE OF O2 BY PULMONARY CAPILLARY BLOOD
• Alveolar PO2 = 104 mmHg
• Pulmonary Arterial PO2 = 40 mmHg
• Difference => 104-40 = 64 mmHg
• Therefore, along the Pressure Gradient,
O2 diffuses through the Alveolo-Capillary
Membrane causing a rapid rise in PO2 as
blood passes through the capillaries and
becomes equal to alveolar PO2.
• Thus,Pulmonary Venous PO2 =104mmHg

23. TRANSPORT OF OXYGEN IN THE ARTERIAL BLOOD
• 98% of blood enters the left Atrium 
Oxygenated up to a PO2 of about 104
mmHg
• Shunt Flow: 2 percent  Shunt Flow
• Venous admixture of blood  PO2
change 104 to 95 mmHg

24. PULMONARY SHUNTING
• SHUNTING = PERFUSION WITHOUT VENTILATION.
• Pulmonary shunt is that portion of the cardiac
output that enters the left side of the heart
without coming in contact with an alveolus.
“True” Shunt – No contact
• Anatomic shunts (Thebesian, Pleural, and
Bronchial Veins)
• Cardiac anomalies
“Shunt-Like” (Relative) Shunt
• Some ventilation, but not enough to allow for
complete equilibration between alveolar gas and
perfusion.
Shunts are refractory to oxygen therapy

25. VENOUS ADMIXTURE
• Venous admixture is the mixing of
shunted,non-reoxygenated blood with
reoxygenated blood distal to the alveoli
resulting in a reduction in:
– PaO2
– SaO2
• Normal Shunt: 3 to 5%
• Shunts above 15% are associated with
significant hypoxemia.

26. EFFECT OF VENOUS ADMIXTURE

27. DIFFUSION OF O2 FROM PERIPHERAL CAPILLARIES TO THE CELLS
• O2 is contantly used by the cells,and thereby PO2 in
peripheral tissue cells remains lower in the peripheral
capillaries at the venous end.The arterial PO2 of 95
mmHg is thus reduced to PO2 of around 40mmHg at the
venous end of the capillaries.
• There is considerable distance between capillaries and
cells . Therefore, cellular PO2 ranges b/w 5-40mmHg
(average 23mmHg).
• Only 1-3mmHg of O2 pressure normally required for full
support of chemical processes that incorporates O2 in
the cell.{PASTEUR POINT – Critical mitochondrial PO2
below which aerobic metabolism cannot occur.Normally
it ranges from 1.4 to 2.3 mm Hg}
• Low intracellular PO2 of 23 mmHg is enough and
provides large safety factor.

28. DIFFUSION OF O2 FROM PERIPHERAL CAPILLARIES IN TO TISSUE FLUID

29. OXYGEN UTILIZATION
• Arterial Blood
- 100 ml of blood combines with 19.4ml of O2
– Po2 95 mmHg
– %Hb saturation 97%
• Venous Blood
- 100 ml of blood combines with 14.4ml of O2
– Po2 40 mmHg
– % Hb saturation 75%
• Thus, 5ml of O2 is transported by each 100
ml of blood through tissues per cycle(250
ml/5L/ min).

30. Summary of Gas Exchange in
Lungs & Tissues

31. THE OXYGEN DISSOCIATION CURVE(ODC)
• Reveals the amount of Haemoglobin
saturation at different PO2 values.

32. CHARACTERISTICS OF THE CURVE
Sigmoid Shaped Curve.
The amount of oxygen that is saturated on the
hemoglobin (SO2) is dependent on the amount
dissolved (PO2).
Amount of O2 carried by Hb rises rapidly upto
PO2 of 60mmHg(Steep Slope) but above that
curve becomes flatter(Flat Slope).
Combination Of 1st Heme with O2 increases
affinity of 2nd
Heme for the 2nd
O2 and so on. It is
known as “Positive Co-Operativity”.

33. THE OXYGEN DISSOCIATION CURVE
In the lungs the partial
pressure is approximately
100mm Hg at this Partial
Pressure haemoglobin has
a high affinity to 02 and is
98% saturated.
In the tissues of other
organs a typical PO2 is 40
mmHg here haemoglobin
has a lower affinity for O2
and offloads O2 to the
tissues.

34. 34
THE “P50”
• A common point of reference on the
oxygen dissociation curve is the P50.
• The P50 represents the partial pressure at
which the hemoglobin is 50% saturated
with oxygen, typically 26.6 mm Hg in
adults.
• The P50 is a conventional measure of
hemoglobin affinity for oxygen.

35. 35
SHIFTS IN THE P50
• In the presence of disease or other conditions
that change the hemoglobin’s oxygen affinity
and, consequently, shift the curve to the right or
left, the P50 changes accordingly.
• An increased P50 indicates a rightward shift
of the standard curve, which means that a
larger partial pressure is necessary to
maintain a 50% oxygen saturation, indicating
a decreased affinity.
• Conversely, a lower P50 indicates a leftward
shift and a higher affinity.

36. FACTORS AFFECTING ODC

37. 37
RIGHT SHIFT
• Right shift decrease the loading of oxygen onto
Hb at the Alveolo-Capillary membrane.
• The total oxygen delivery may be much lower
than indicated by a particular Pao2 when the
patient has some disease process that causes a
right shift.
• Right shift curves enhance the unloading of
oxygen at the tissue level.

38. 38
LEFT SHIFT
• Left shift curves enhance the loading capability
of oxygen at the Alveolo-Capillary membrane.
• The total oxygen delivery may be higher than
indicated by a particular PaO2 when the patient
has some disease process that cause a left shift.
• Left shift curves decreases the unloading of
oxygen at the tissue level.

40. FACTORS AFFECTING DISSSOCIATION
BLOOD TEMPERATURE
• increased blood temperature
• reduces haemoglobin affinity for O2
• hence more O2 is delivered to warmed-up
tissue
Respiratory Response to Exercise
BLOOD Ph
• lowering of blood pH (making blood
more acidic)
• caused by presence of H+
ions from lactic
acid or carbonic acid
• reduces affinity of Hb for O2
• and more O2 is delivered to acidic sites
which are working harder
CARBON DIOXIDE CONCENTRATION
• the higher CO2 concentration in tissue
• the less the affinity of Hb for O2
• so the harder the tissue is working, the
more O2 is released

41. HEMOGLOBIN & MYOGLOBIN
• Myoglobin is single
chained heme pigment
found in skeletal
muscle.
• Myoglobin has an
increased affinity for
O2 (binds O2 at lower
Po2)
• Mb stores O2
temporarily in muscles
& acts as a reserve in
muscles, which can be
used during exercise.

43. ROLE OF 2,3-DPG
(DiPhosphoGlycerate):
•2,3 DPG is an
organic phosphate
normally
found in the RBC.
•Produced during
Anaerobic
glycolysis in
RBCS.

44. CONTD..
• 2,3 DPG has a tendency to bind to β chains of
Hb and thereby decrease the affinity of
Hemoglobin for oxygen.
HbO2 + 2,3 DPG → Hb-2,3 DPG + O2
• It promotes a rightward shift and enhances
oxygen unloading at the tissues.
• This shift is longer in duration than that due to
[H+] or PCO2 or temperature.

45.  The levels increase with:
• Cellular hypoxia.
• Anemia
• Hypoxemia secondary to
COPD
• Congenital Heart
Disease
• Ascent to high altitudes
 The levels decrease with:
• Septic Shock
• Acidemia
• Stored blood has No
DPG after 2 weeks of
storage.
• In banked blood,the 2,3-
BPG level falls and the
ability of this blood to
release O2 to the tissues
is reduced.

46. •
EFFECTS OF ANEMIA & CARBON MONOXIDE ON
THE OXYGEN DISSOCIATION CURVE
• ↓O2 content.
• SaO2remains normal
• Carbon Monoxide [CO]
affinity of Hb for CO is 250
fold relative to O2 competes
with O2 binding
• L shift- interfere with O2
unloading at tissues causing
severe tissue hypoxia.
• Sigmoidal HbO2 curve
becomes Hyperbolic.

47. HAEMOGLOBIN SATURATION AT HIGH ALTITUDES
Lungs at sea level:
PO2 of 100mmHg
haemoglobin is 98%
SATURATED
Lungs at high
elevations: PO2
of 80mmHg,
haemoglobin 95
% saturated
At pressures above
60mm Hg, the standard
dissociation curve is
relatively flat.
This means the oxygen
content does not change
significantly even with
large changes in the
partial pressure of
oxygen.

48. HAEMOGLOBIN SATURATION DURING EXERCISE

49. CARBON DIOXIDE
• Volatile waste product of aerobic
metabolism.
• Production averages 200 ml/min in resting
adult.
• During exercise this amount may increase
6x.
• Produced almost entirely in the
mitochondria.
• Importance of CO2 elimination lies in the
fact that -Ventilatory control system is
more responsive to PaCO2 changes

50. CARBON DIOXIDE TRANSPORT
• Carbon dioxide also relies on the blood for
transportation. Once carbon dioxide is
released from the cells, it is carried in the
blood primarily in three ways..
Dissolved in plasma.
As bicarbonate ions resulting from the
dissociation of carbonic acid.
Bound to haemoglobin.

51. When CO2 molecules diffuse from the
tissues into the blood
• 7% remains dissolved in plasma
• 23% combines in the erythrocytes with
deoxyhemoglobin to form carbamino
compounds.
• 70% combines in the erythrocytes with
water to form carbonic acid, which then
dissociates to yield bicarbonate and H+
ions.

52. MOST CO2 TRANSPORTED
AS BICARBONATE (HCO3-
)*

53. CHLORIDE SHIFT AND
REVERSE CHLORIDE SHIFT
• Most of the bicarbonate then moves out of the
erythrocytes into the plasma in exchange for Cl-
ions &
the excess H+
ions bind to deoxyhemoglobin,known as
Chloride Shift.
• The reverse occurs in the pulmonary capillaries and CO2
moves down its concentration gradient from blood to
alveoli,known as Reverse Chloride Shift.
• As a result of the shift of chloride ions into the red cell
and the buffering of hydrogen ions onto reduced
haemoglobin, the intercellular osmolarity increases
slightly and→→ water enters causing the cell to swell
→→ an increase in mean corpuscular volume (MCV)
• Hematocrit of venous blood is 3%>arterial
• Venous RBC are more fragile
• Cl content of RBCs V>A

54. CARBON DIOXIDE TRANSPORT

55. CARBON DIOXIDE DISSOCIATION CURVE
Total CO2 carriage in
the blood depends on
the three blood-gas
parameters:
– PCO2
– Plasma pH
– PO2
Carbon dioxide
dissociation curves
relate PaCO2 to the
amount of
carbon dioxide carried in
blood

56. Lower the
saturation of
Hb with O2 ,
larger the
CO2 conc for a
given
PaCO2.
CO2 curve is
shifted to
right by increase
in SpO2

57. Graph illustrates the difference
between the content in blood of
oxygen and carbon dioxide with
change in partial pressure
•CO2 content rises throughout
the increase in partial
pressure.
• O2content rises more steeply
until a point at which the hb is
fully saturated. After that, the
increase is small because of
the small increased amount in
solution.
• Consequently, the CO2 curve
is more linear than the O2Hb
dissociation curve.

58. Deoxygenation of Hb
↑ qty of CO2 bound to
Hb.
For any given PCO2, the
blood will hold more CO2
when the PO2 has been
diminished.
Reflects the tendency
for an increase in PO2 to
diminish the affinity of
hemoglobin for CO2.
HALDANE EFFECT

59. MECHANISM OF HALDANE EFFECT
Combination of oxygen with hemoglobin in the lungs
causes the hemoglobin to become a stronger acid.
Therefore:
1) The more highly acidic hemoglobin has less tendency to
combine with CO2 to form CO2 Hb
2) The increased acidity of the hemoglobin also causes it to
release an excess of hydrogen ions thus causing a further
rise in the ph and decreased tendency of CO2 to combine
with hemoglobin in the presence of oxygen.

60. INTERACTION BETWEEN CO2 AND
O2 TRANSPORTATION
1. Bohr effect

61. 2. Haldane effect

62. DIFFERENCES BETWEEN
BOHR’S AND HALDANE’S
EFFECT
• BOHR’S EFFECT
1.It is the effect by
which the presence
of CO2 decreases
the affinity of Hb
for O2
• HALDANE EFFECT
1.It is the effect by
which combination of
O2 with Hb displaces
CO2 from Hb

63. 2. Was postulated by
Bohr in 1904.
3. Occurs at tissues
and systemic
capillaries.
4. In tissues, body
metabolism causes
↑PCO2(45 mmHg) &
↓ PO2(40mmHg)
with respect to
arterial PCO2 and
PO2.
2. Described by John
Scott Haldane in
1860.
3. Occurs at alveolar
and pulmonary
capillaries.
4. In lungs,
Hb+O2HbO2
HbO2 has low
tendency to
combine with CO2.

64. • CO2 enters the
blood and O2
released from
blood to tissues..
• Shifting O2
disosiciation curve
to right and
unloading O2 to
the tissues.
• O2+HbH+ and
CO2
• H+ + HCO3-
H2CO3H2O
+CO2..
• CO2 is thus
released from
blood to alveoli to
be expelled out.

65. tissues