2. Physiological Causes of Hypoxemia
Hypoventilation
Diffusion impairment
Ventilation-perfusion (V/Q) mismatching
Right-to-left shunting versus dead space
Reduced inspired oxygen tension (altitude)
3. O2 partial pressures from air to tissues
âą PO2 falls as gas moves
from the air to
mitochondria
âą Determinants of PO2
â Rate of removal of
oxygen by pulmonary
capillary blood
âą Set by metabolic
demands of the tissues
â Rate of replenishment
by alveolar ventilation
5. PAO2
= FiO2 x [Patm - PH2O] -
PaCO2
R
Alveolar Gas Equation
** A-a = 149 â (PaO2 + PaCO2 + .25PaCO2)**
**Use this form if the patient is NOT on supplemental oxygen
(on âroom airâ)
7. PAO2
= FiO2
x [Patm - PH2O] -
PaCO2
R
.
PaCO2 =
VCO2 x K
VA
.
If alveolar ventilation decreases, the PaCO2 risesâŠ
And, if PaCO2 rises, PAO2 falls (and as a result PaO2 falls
similarly)
9. Diffusion Impairment
âą For oxygen to reach
the pulmonary
capillary, it must
traverse the
interstitium
âą Determinants include
thickness of the
interstitium and the
rate of capillary blood
flow
10. Diffusion Impairment
âą For oxygen to reach
the pulmonary
capillary, it must
traverse the
interstitium
âą Determinants include
thickness of the
interstitium and the
rate of capillary blood
flow
11. Diffusing capacity is further determined by both the capacity of the
membrane, the volume of blood in the capillaries, AND the rate of reaction
between the oxygen molecule and hemoglobin
14. Effect of right-to-left shunt on arterial
oxygenation
Note, on graph B, that in the presence of a 50% R-to-L shunt, increasing the FiO2 from
room air to 100% (or PIO2 from 150 to 760) results in only an increase in PaO2 by 12!
17. Types of Dead Space
A. Anatomic
The only areas
where gas
exchange does not
take place are the
conducting airways
B. Physiologic
Not all ventilation
units are coupled
to pulmonary
blood flow
18. Dead Space and
Ventilatory Demand
Point A â Normal Values
for VD/VT, PaCO2, and VE
Point B â Effect on VE when
VD/VT increases from 0.3
to 0.75. Dramatic increase
in ventilation required to
maintain a normal PaCO2
Point C â To push the
PaCO2 even lower, the
ventilatory requirement
increases exponentially for
a given VD/VT
19. In case youâre wonderingâŠ
âą V/Q mismatching rarely causes a disruption in
PaCO2. Why?
âą Ventilatory drive (stimulated by
chemoreceptors) is exquisitely sensitive to
rising PaCO2
âą Further, this increased ventilation is âwastedâ
on normal alveolar units
â âalveolar dead spaceâ
21. Interval Summary
âą Primary causes of hypoxemia
â V/Q mismatching
âą And, the extreme example of the Rï L shunt
â Diffusion impairment
â Hypoventilation
âą Worsening dead space ventilation results in
increased alveolar ventilation
â Little impact on PO2
22. Disease States and Hypoxemia
âą COPD
âą Pulmonary Edema
âą Fibrosing ILD, such as IPF
30. Hypoxemia in Pulmonary Edema
Ventilation obstructed by
edema fluid, lowering
alveolar PO2
31. Hypoxemia in Fibrosing ILD
A combination of V/Q
mismatching as well as
diffusion impairment
Ventilation and
perfusion are regionally
reduced by the
destructive fibrotic
disease
33. Diffusing capacity is determined by both the capacity of the membrane, the
volume of blood in the capillaries, AND the rate of reaction between the
oxygen molecule and hemoglobin
34. PO2 against time in the pulmonary capillary. Note that with exercise/exertion, the
time for oxygenation reduces drastically (âdiffusion limitationâ)
35. Summary
âą In clinical practice, three primary physiological
causes of hypoxemia
â Hypoventilation
â V/Q mismatching (primarily via R->L shunting)
â Impaired gas diffusion
âą In reality, most disease states lead to hypoxemia
by more than one mechanism
âą Keeping the alveolar gas and alveolar ventilation
equations handy can go a long way in
determining the cause of and response to
hypoxemia
36. PAO2
= FiO2
x [Patm - PH2O] -
PaCO2
R
.
PaCO2 =
VCO2 x K
VA
.
Expired minute ventilation
(or ventilatory demand)
(1-VD/VT)
VA
.
=