2. Antoine Lavoisier was an 18th-century French scientist who
was the first to identify oxygen as the essential element for
metabolism.
The requirements of the oxygen transport system from the
atmosphere to all organs, tissues, cells and mitochondria.
This combined oxygen transport system is known as
OXYGEN CASCADE.
When the system fails to supply oxygen to meet the
prevailing demand, a state of hypoxia is said to exist
3. OXYGEN CASCADE
It describes the process of decreasing oxygen tension from
atmosphere to mitochondria.
Atmospheric air
↓
Alveoli
↓
Arterial blood
↓
Tissue capillaries
↓
Mitochondria
4. Atmospheric air
Partial pressure of O2 in saturated moist air
(PiO2)
PiO2 = FIO2 (PB – PH2O)
At sea level:
Water vapour pressure at body temp =
47mmHg . Thus, Pressure exerted by gas in
saturated moist air = 760-47 = 713mmHg.
So the inspired oxygen partial pressure
= [ 0.21 (760 – 47) ]
= 149 mmHg
This is the starting point of O2 cascade.
5. Alveoli
Alveolar partial pressure
Partial pressure of alveolar oxygen(PAO2 ) is
calculated by alveolar gas equation PAO2= PiO2-
PACO2/R
PaCO₂ = PACO₂ ( 40mmHg ) as CO₂ is freely
diffusible.
PAO2 =149-(40/0.8)~100mmHg.
6. ALVEOLI TO BLOOD
Alveolar PAO2 is 100mmHg. Blood returning from
tissues to heart has low PO2 (40mmHg).
So oxygen diffuses from alveoli to pulmonary
capillaries.
After oxygenation,blood moves to pulm.
veins→left side of heart→ arterial system →
systemic tissues.
In a perfect lung pO₂ of pulm. Venous blood
would be equal to pO₂ in the alveolus
7. OXYGEN DELIVERY TO TISSUE (
DO2 )
DO2 = [(1.34 x HbxSaO2)+(0.003xPaO2)] x Q
10
O2 delivery to tissues depends on
Hb concentration
O2 binding capacity of Hb
Saturation of Hb
Amount of dissolved O2
cardiac output (Q).
8. UNLOADING OF O2 AT TISSUE
LEVEL
Initially the dissolved O2 is consumed.
Then the sequential unloading of Hb bound O2
occurs.
Transport of O2 from the capillaries to tissues is
by simple diffusion.
Pasteur point is the critical PO2 at which
delivered O2 is utilised by the tissue & below
which the O2 delivery is unable to meet the tissue
demands.
9. Oxygen cascade refers to the progressive
decrease in the partial pressure of oxygen from
the ambient air to the cellular level.
PO2 in inspired air 150-160 mm Hg
PO2 in alveolar gas (PAO2) 100-110 mm Hg
PO2 in arterial blood (PaO2) 90-100 mm Hg
PO2 in Capillary blood 50-80 mm Hg
PO2 in tissues 30-50 mm Hg
PO2 in cell mitochondria 10-20 mm Hg
10. Factors affecting oxygenation at
various levels in O2 cascade:
PARTIAL PRESSURE AFFECTED BY:
Inspired oxygen PiO2 Barometric pressure (Pb);
FiO2
Alveolar gas PAO2 Oxygen consumption VO2
Alveolar ventilation VA
Arterial blood PaO2 Dead space ventilation
Shunt Decreased V/Q
Cellular PO2 Cardiac output CO
hemoglobin
11. Dead Space Ventilation
Where ventilation is excessive relative to
pulmonary capillary blood flow.
In normal subjects, dead space ventilation (VD)
accounts for 20% to 30% of the total ventilation
(VT); i.e., VD/VT = 0.2 to 0.3
Dead space ventilation increases in the following
situations: 1. When the alveolar–capillary
interface is destroyed; e.g., emphysema
2. When blood flow is reduced; i.e., low cardiac
output
3. When alveoli are overdistended; e.g., during
positive-pressure ventilation
12. Intrapulmonary Shunt
The excess blood flow, known as intrapulmonary
shunt, does not participate in pulmonary gas
exchange.
V/Q ratio below 1.0
The fraction of the cardiac output that represents
intrapulmonary shunt is known as the shunt
fraction. In normal subjects, intrapulmonary shunt
flow (Qs) represents less than 10% of the total
cardiac output (Qt), so the shunt fraction (Qs/Qt)
is less than 10%.
13. Intrapulmonary shunt fraction is increased in the
following situations:
1. When the small airways are occluded; e.g.,
asthma
2. When the alveoli are filled with fluid; e.g.,
pulmonary edema, pneumonia
3. When the alveoli collapse; e.g., atelectasis
4. When capillary flow is excessive; e.g., in
nonembolized regions of the lung in pulmonary
embolism.
15. 5. The A-a PO2 Gradient
6.PaO2/FIO2 Ratio
7. Mixed venous saturation of oxygen &
central venous oxygen saturation
METABOLIC PRODUCT
8. Lactate
9. Arterial Base Deficit
GASTRIC TONOMETRY
NEAR INFRARED SPECTROSCOPY (NIRS)
16. Oxygen Delivery (DO2)
The rate of O2 transport from the heart to the
systemic capillaries is called the oxygen delivery
(DO2)
DO2 = CO × CaO2 × 10 (mL/min)
(The multiplier of 10 is used to convert the CaO2
from mL/dL to mL/L.)
The DO2 in healthy adults at rest is 900–1100
mL/min, or 500–600 mL/min/m2 when adjusted
for body size.
17. Oxygen uptake (VO2).
The rate of O2 transport from the systemic capillaries
into the tissues is called the oxygen uptake (VO2).
The VO2 can be described as the product of the
cardiac output (CO) and the difference between
arterial and venous O2 content (CaO2 – CvO2).
VO2 = CO × (CaO2 – CvO2) × 10 (mL/min)
This equation is a modified version of the Fick
equation for cardiac output (CO = VO2/CaO2 –
CvO2). The CaO2 and CvO2 in equation share a
common term (1.34× [Hb]), so the equation can be
restated as: VO2 = CO × 1.34 × [Hb] × (SaO2 –
SvO2) × 10
The VO2 in healthy adults at rest is 200–300 mL/min,
or 110–160 mL/min/m2 when adjusted for body size
18. The two conditions associated with a low VO2 are
a decreased metabolic rate (hypometabolism)
and inadequate tissue oxygenation.
Hypometabolism is uncommon in ICU patients,
an abnormally low VO2 (<200 mL/min or <110
mL/min/m2) can be used as evidence of
inadequate tissue oxygenation.
VO2 may be a more sensitive marker of
inadequate tissue oxygenation than the serum
lactate level.
19. Oxygen Extraction
The fractional uptake of O2 into tissues
It is the ratio of O2 uptake (VO2) to O2 delivery
(DO2).
O2ER = VO2/DO2
O2ER = (SaO2 – SvO2)/SaO2.
The VO2 is normally about 25% of the DO2, so
the normal O2ER is 0.25 (range = 0.2–0.3). Thus,
only 25% of the O2 delivered to the capillaries is
taken up into the tissues when conditions are
normal.
The point where O2 extraction is maximal is the
anaerobic threshold.
21. 1. The normal (SaO2 – SvO2) is 20% to 30%.
2. An increase in (SaO2 – SvO2) above 30%
indicates a decrease in O2 delivery (i.e., usually
anemia or a low cardiac output).
3. An increase in (SaO2 – SvO2) that
approaches 50% indicates either threatened or
inadequate tissue oxygenation
4. A decrease in (SaO2 – SvO2) below 20%
indicates a defect in O2 utilization in tissues,
which is usually the result of inflammatory cell
injury in severe sepsis or septic shock.
22. Venous Oxygen Saturation
Mixed venous oxygen saturation (SvO2)
The SvO2 is ideally measured in mixed venous
blood in the pulmonary arteries, which requires a
pulmonary artery catheter.
The normal range for SvO2 in pulmonary artery
blood is 65% to 75%.
Continuous SvO2 monitoring is associated with
spontaneous fluctuations that average 5%. A
change in SvO2 must exceed 5% and persist for
longer than 10 minutes to be considered a
significant change.
23. Central Venous O2 Saturation
(ScvO2)
The O2 saturation in the superior vena cava,
known as the “central venous”.
An alternative to the mixed venous O2 saturation
(SvO2) because it eliminates the need for a PA
catheter.
Scvo2 is usually 2-3% lower than Svo2. This is
because the lower half of the body extracts less
oxygen and the brain extracts more oxygen than
other organs of the body.
Normal oxygen extraction is 25–30%
corresponding to a ScvO2 >65%
24. situations where ScvO2 > SvO2:
-> anaesthesia – because of increase in CBF and
depression of metabolism
-> TBI where cerebral metabolism depressed
-> shock – because of diversion of blood from
splanchnic circulation + increased oxygen
extraction and therefore IVC saturation
decreases.
25.
26. The A-a PO2 Gradient
An indirect measure of ventilation–perfusion
abnormalities.
The normal A-a PO2 gradient rises steadily with
advancing age. It ranges from 5 to 25 mmHg
breathing room air.
The normal A-a PO2 gradient increases 5 to 7
mm Hg for every 10% increase in FIO2.
27. The PaO2/FIO2 Ratio
The PaO2/FIO2 ratio is used as an indirect
estimate of shunt fraction. The following
correlations have been reported
PaO2/FIO2 Qs/Qt
<200 >20%
>200 <20%
28. Lactate
Product of anaerobic glycolysis.
LEVELS
1. normal range: 0.6-1.8mmol/L
2. hyperlactaemia: a level from 2 to 5 mmol/L
3. severe lactic acidosis: > 5 mmol/L
4. high mortality with lactate > 8mmol/L
PHYSIOLOGY
1. Daily production: ~ 1500 mmol of lactate each day (
mmol of lactate each day (15 to 30 mmol/kg per
day) .
2. all tissues can produce lactate under anaerobic
conditions
3. Metabolized mainly by the liver ( Cori cycle)
30. Lactic acidosis occurs whenever there is an
imbalance between the production and use of
lactic acid.
Causes of Lactic acidosis
•Type A
•Type B
31.
32. Arterial Base Deficit
“base deficit” is considered a more specific
marker of metabolic acidosis than the serum
bicarbonate.
The normal arterial base deficit is ≤2 mmol/L;
increases above 2 mmol/L are classified as mild
(2 to 5 mmol/L), moderate (6 to 14 mmol/L), and
severe (≥15 mmol/L).
Arterial base deficit has been a popular marker of
impaired tissue oxygenation in acute surgical
emergencies, especially trauma
33. GASTRIC TONOMETRY
Technique used to assess regional perfusion.
Assesses splanchnic perfusion based on
stomach’s mucosal pH by measuring gastric
luminal PCO2 using a fluid filled balloon
permeable to gases.
Luminal CO2 reflects intramucosal CO2.
Several limitations to using gastric tonometry
routinely: – takes about 90 minutes for CO2 to
equilibrate between the balloon and the lumen –
Luminal CO2 may be affected by acid secretion
and feeding – No convincing evidence to support
its routine use in the intensive care as several
trials have failed to show benefit in using this form
of monitoring
34. NEAR INFRARED SPECTROSCOPY
(NIRS)
A noninvasive method of measuring the venous
O2 saturation in tissues using the optical
properties of hemoglobin in the oxygenated
(HbO2) and dexoxygenated (Hb) state.
The most exciting feature of NIRS is the potential
to monitor mitochondrial O2 consumption.
