Oxy gen T r anspor t

& Del iver y

Dr Prashant S Agarwal
Dr Ashok Jadon
Deptt of Anaesthesia
Learning O bjective s

 To understand the basic physiology of oxygen

transport.
 Oxygen Flux
 Oxygen delivery to tissues
 Extraction ratio
 Oxygen debt
 How O2 therapy works
 An aero bic ? So
What?
Inadequate
Cellular
Oxygenation

Inadequate
Anaerobic Lactic Acid
Energy
Metabolism Production
Production

Metabolic Metabolic
Cell Death!
Failure Acidosis
Tourniquet application Vs
Carotid Clamping…..
 Tourniquet is well tolerated for certain
period but not carotid clamping

 In muscles these ions easily diffuse out

causing metabolic acidosis.
 In brain the BBB prevents this diffusion
leading to intracellular acidosis and
structural damage.
Fate o f Ox yg en

 1. From atmosphere to lung

capillaries.

 2. Oxygen in blood.

 3 Cellular Function.
 PiO2 Nose : PB-47)x FiO2
 PiO2 Alveoli: (PB-47)x FiO2- PaCO2/R

 : Arterial pressure: PaO2

 Alveolar-arterial Dissociation:=Alv-art
 Sea Level Pao2: 760 x0.21=159 mmhg.
 Nose: ( 760-47)x .21=149 mmhg.( water Vapor)
 At Alveoli: 149- 40/0.8=100 mmhg.( C02).
 At Arterial level:90 mmhg ( gradiant 5-10mmhg)
 At venous : 47 mmhg
 Mitrochondria: 35-40 mmhg
 Interference to the delivery of oxygen at any point in the
cascade, significant injury can occur downstream
Lung to Blo od

 Four factors influence transmission of

oxygen from the alveoli to the capillaries
 1. Ventilation perfusion (V/Q) mismatch,
 2. Right to left shunt,
 3. Diffusion defects,
 4. Cardiac output.
Esse ntia ls of Ga s
Ex change
PiO2 =
150 mmHg

PALV O2= 100 mmHg

Due to CO2 added
 V/Q mismatch
Zone 1 PB=0
PA
Pa Pv PA>Pa>Pv
Low Flow Flow=∆P/R

PA Zone 2
Pa Pv
Pa>PA>Pv
Waterfall
PA<0

PA Zone 3 O2
venous arterial
Pa Pv Pa>Pv>PA
Hi Flow CO2
Ventilation Perfusion Ratios
PO2 = 150
PCO2 = 0

PO2 = 40 PO2 = 100 PO2 = 150

PCO2 = 45 PCO2 = 40 PCO2 = 0
No flow

CO2 = 45
. . .
Low VA/Q Normal VA/Q High VA/Q
 PO2 = 40
PCO2 = 45
PO2 = 100
50 PCO2 = 40
.
Low VA/Q Base
PCO2 (mm Hg)

.
Normal VA/Q
PO2 = 150
PCO2 = 0

Apex

.
High VA/Q
50 100 150
PO2 (mm Hg)
Sh unts
Sh unt- Wh y O2 dose
not wo rk
Ox ygen Co ntent

 Amount of O2 carried by 100 ml of

blood
 In two forms –
 Bound to Hb 98%
 Dissolved in plasma 2%
 N = 20 ml of O2 in 100 ml blood
Oxygen
content
98% O2 is bound to Hb.
CaO2 = ( Hb 1.34  SaO2 )


2% Dissolved O2
( PaO2  0.003 ml )
Ox ygen t ra nsp ort
Look at the graph
 Hb becomes almost fully
saturated with oxygen at
high partial pressures
such as is found in the
lungs
 Oxyhaemoglobin
dissociates under low
partia pressures such as
found in respiring tissue.
Ox ygen t ra nsp ort

Why is the curve S shaped?

 Each molecule of Hb has four haem
groups
 When the first oxygen combines with the
first haem group the shape of the Hb
molecule becomes distorted
 This makes it easier for the other three
oxygen molecules to bind to the other
haem groups
Hb O2 Content by 70 folds but
in PO2 …..
Ox ygen d is sociation
curve .
PaO2 SATURATION O2
content
HB% 12 Normal
SAT 100%

HB% 12
SAT 50% ↓
HB 6
SAT 100% ↓
HB 13
SAT 90%
↓or N
 PAO2 OXY (Sat)
C. SaO2 98%
A.C.I. HAEMOGLOBI
D. N
O.

PaO2 Delivery
2 % Dissolved
Oxygen Of
Oxygen
CaO2
Content of oxygen To
Ml/100 of blood
O2 Tissues
Cardiac output DaO2
A.C.I.( Alveolar capillary interface)
O2 F lu x ( deli ve ry)
 Amount of O2 leaving the left ventrical per
minute
 Overall oxygen delivery = arterial oxygen
content x cardiac output
 DO2 = CO x CaO2
 DO2 = C.O. x Hb saturation x 1.31 x Ηb conc
100 100
= 5500 x 95 x 1.31 x 14.5
100 100
 DO2 = 800 – 1200 ml/min
If H b 7 .5 gm%
O2 flux = 513 ml/min

If C.O. is also to 3000 ml

O2 flux = 580 ml/min

If both are then O2 flux = 280ml/min

O2 Up ta ke

 Oxygen Uptake VO2 : Is a function of

Cardiac output
 Difference in oxygen content b/w arterial
and venous blood
 VO2 = CO x 1.34 x Hb (SaO2 – SvO2) 10

 VO2 = 200 – 300 ml/min

 Mo re unloaded wit h
mo re n eed

Resting cell PO2

40 mmHg

Working cell PO2

20 mmHg
Ox ygen Ex traction
Ra tio (O2 ER)
 Is the ratio of oxygen uptake to delivery. Usually 20-
30%
 O2 ER = VO2/DO2
 Uptake is kept constant by increasing extraction when
delivery drops
 Critical Oxygen Delivery (DO2crit)
Maximal extraction ~ 50-60%
 Once this is reached a decrease in delivery = decrease
in uptake
 Known as ‘critical oxygen delivery’
 O2 uptake and aerobic energy production is now
supply dependent
Can you remember
why it is important
to warm down after
exercise?
 OXYGEN DEBT
‘The extra amount of oxygen needed to
recover from anaerobic activity
You will develop oxygen debt after about 5
minutes or more of constant exercise.
This is the point when the exercise becomes
ANAEROBIC (without the use of oxygen) and
which has to be paid back later- hence
OXYGEN DEBT.
If the exercise is just AEROBIC (with oxygen)
there will be no oxygen debt.
Estimates of anaerobic effort
• Post-exercise oxygen consumption
Oxygen debt – excessive post-exercise
oxygen consumption - EPOC
• The lactic threshold
The point at which blood lactate begins
accumulate above resting values during
exercise of increasing intensity. The onset of
blood lactate accumulation (OBLA) is a standard
value set at either 2.0 or 4.0 mmol lactate.L-1 O2
and is used as a common reference point.
Expressed as
percentage of Vo2 max – best determinant of
athletes pace in endurance events. Untrained
people – lactate threshold at 50-60% of Vo2-max,
in elite runners at 70-80%, lactate formation
contributes to fatigue
Pa rtia l p ressu re

 The partial pressure gradients for O2 &

CO2 are the key to gas movement.
 However, the amount of both of these
gases would be grossly inadequate if Hb
is not there.
(Ganong 20th ed)
Da lt on’s Law
 In a mixture of ideal gases, each gas has a
partial pressure which is the pressure which the
gas would have if it alone occupied the volume.
The total pressure of a gas mixture is the sum of
the partial pressures of each individual gas in
the mixture.
 Thus, if the normal pressure of atmospheric
gases is 760 mmHg and there is 21% oxygen,
the partial pressure of oxygen is 760 × 0.21 =
160 mmHg.
What we breath..?

 160 mmHg
O2
160 mmHg

H2 O
CO2
Shunts

35-40mmHg

47mmHg
 Pa st ure Po in t….
 Critical PO2 (1-2mmHg) during hypoxia
where aerobic metabolism fails in
mitocondria.

O2 therapy
 To increase the FiO2 & PaO2
 If breathing 100% O2
 Then FiO2 is 1 & PaO2 610 mmHg
160 mmHg

35-40mmHg

47mmHg
 1. The oxygen cascade describes the process of declining oxygen tension
from atmosphere to mitochondria.

 2. The amount of oxygen in the blood is calculated using the formula:

[1.34 x Hb x (SaO2/100)] + 0.003 x PO2 = 20.8ml

 3. The delivery of oxygen to the tissues per minute is calculated from:

DO2 = [1.39 x Hb x SaO2 + (0.003 x PaO2)] x Q

 4. Tissue oxygen extraction is calculated by subtracting mixed venous

oxygen content from arterial oxygen content.

 5. The Oxyhemoglobin dissociation curve describes the non-linear

tendency for oxygen to bind to hemoglobin: below a SaO2 of 90%, small
differences in hemoglobin saturation reflect large changes in PaO2 Right
to left shunting causes hypoxemia resistant to oxygen therapy. .
 6. Right to left shunt causes hypoxemia unresponsive
to oxygen therapy Diffusion defects and ventilation
perfusion mismatches cause hypoxemia, responsive to
exogenous oxygen and positive pressure ventilation.

 7. The objective of oxygen therapy is to give the patient

as much oxygen as is required to return the PaO2 to
what is normal for the particular patient.

 8. Oxygen is given thru fixed and variable performance

devices.