Physiology of Hypoxemia
Corey D. Kershaw, M.D.
February 20, 2015
Physiological Causes of Hypoxemia
Hypoventilation
Diffusion impairment
Ventilation-perfusion (V/Q) mismatching
Right-to-left shunting versus dead space
Reduced inspired oxygen tension (altitude)
O2 partial pressures from air to tissues
• PO2 falls as gas moves from the air to mitochondria
• Determinants of PO2
– Rate of removal of oxygen by pulmonary capillary blood• Set by metabolic
demands of the tissues
– Rate of replenishment by alveolar ventilation
Alveolar Ventilation Equation
.
PaCO2 = VCO
2x K
VA
.
Expired minute ventilation
(or ventilatory demand)(1-VD/VT)
VA
.
=
PAO2
= FiO2 x [Patm - PH2O] -PaCO
2
R
Alveolar Gas Equation
** A-a = 149 – (PaO2 + PaCO2 + .25PaCO2)**
**Use this form if the patient is NOT on supplemental oxygen (on “room air”)
Why is there a “normal” A-a gradient?
PAO2
= FiO2
x [Patm - PH2O] -PaCO
2
R
.
PaCO2 =VCO
2x K
VA
.
If alveolar ventilation decreases, the PaCO2 rises…
And, if PaCO2 rises, PAO2 falls (and as a result PaO2 falls similarly)
Hypoventilation as a cause of hypoxemia
Alveolar Gas Equation, graphically
Diffusion Impairment
• For oxygen to reach the pulmonary capillary, it must traverse the interstitium
• Determinants include thickness of the interstitium and the rate of capillary blood flow
Diffusion Impairment
• For oxygen to reach the pulmonary capillary, it must traverse the interstitium
• Determinants include thickness of the interstitium and the rate of capillary blood flow
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
Dead space
Shunt
There are different degrees of V/Q mismatching
Effect of shunt on PO2
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!
Hypoxemic vasoconstriction
Dead space
Shunt
There are different degrees of V/Q mismatching
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
Dead Space and Ventilatory Demand
Point A – Normal Values for VD/VT, PaCO2, and VE
Point B – 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 – To push the PaCO2 even lower, the ventilatory requirement increases exponentially for a given VD/VT
In case you’re wondering…
• V/Q mismatching rarely causes a disruption in PaCO2. Why?
• Ventilatory drive (stimulated by chemoreceptors) is exquisitely sensitive to rising PaCO2
• Further, this increased ventilation is “wasted” on normal alveolar units
– “alveolar dead space”
Alveolar ventilation/PaO2 relationship
Increasing alveolar ventilation has very little impact on PO2
(“alveolar dead space”)
Interval Summary
• Primary causes of hypoxemia
– V/Q mismatching
• And, the extreme example of the RL shunt
– Diffusion impairment
– Hypoventilation
• Worsening dead space ventilation results in increased alveolar ventilation
– Little impact on PO2
Disease States and Hypoxemia
• COPD
• Pulmonary Edema
• Fibrosing ILD, such as IPF
Hypoxemia in COPD
Regional differences in gas exchange
V/Q ratio in a normal patient
Hypoxemia in COPD
V/Q ratio in patient with emphysema & chronic bronchitis
V/Q mismatching and changes on PO2
Hypoxemia in Pulmonary Edema
Chiefly due to shunt physiology
Hypoxemia in Pulmonary Edema
Ventilation obstructed by edema fluid, lowering alveolar PO2
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
Hypoxemia in Fibrosing ILD
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
PO2 against time in the pulmonary capillary. Note that with exercise/exertion, the time for oxygenation reduces drastically (“diffusion limitation”)
Summary
• In clinical practice, three primary physiological causes of hypoxemia– Hypoventilation– V/Q mismatching (primarily via R->L shunting)– Impaired gas diffusion
• In reality, most disease states lead to hypoxemia by more than one mechanism
• Keeping the alveolar gas and alveolar ventilation equations handy can go a long way in determining the cause of and response to hypoxemia
PAO2
= FiO2 x [Patm - PH2O] -
PaCO2
R.
PaCO2 = VCO
2x K
VA
.
Expired minute ventilation
(or ventilatory demand)(1-VD/VT)
VA
.
=
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