The alveolar gas equation for calculating PAO2 is essential to
understanding any PaO2 value and in assessing if the lungs are properly
transferring oxygen into the blood. Is a PaO2 of 28 mm Hg abnormal?
How about 55 mm Hg? 95 mm Hg? To clinically interpret PaO2 one has
to also know the patient's PaCO2, FIO2 (fraction of inspired oxygen) and
the PB (barometric pressure), all components of the equation for PAO2:
Despite this undisputed physiologic fact physicians sometimes
make clinical decisions
The abbreviated equation below is useful for clinical purposes; in
this version alveolar PO2 equals inspired PO2 (PIO2) minus arterial PCO2
x 1.2, assuming the R value is 0.8 (and assuming identical values for
arterial and alveolar PCO2. Water vapor pressure in the airways is
dependent only on body temperature and is 47 mm Hg at normal body
temperature (37 degrees C).
Ambient FIO2 is the same at all altitudes, 0.21. It is usually not
necessary to measure PB if you know its approximate average value where
the blood was drawn (e.g. sea level 760 mm Hg; Cleveland 747 mm Hg;
Denver 640 mm Hg). In the abbreviated equation PaCO2 is multiplied by
1.2, a factor based on assumed respiratory quotient (CO2 excretion over
O2 uptake in the lungs) of 0.8; this factor becomes 1.0 when the FIO2 is
1.0.22 The following comments are meant to show how the alveolar gas
equation can be clinically helpful without the need for anything more
than mental calculation.
a) If PIO2 is held constant and PaCO2 increases, PAO2 and
PaO2 will always decrease. Since PAO2 is a calculation based on
known (or assumed) factors, its change is predictable. PaO2, by
contrast, is a measurement whose theoretical maximum value is
defined by PAO2 but whose lower limit is determined by
ventilation-perfusion (V-Q) imbalance, pulmonary diffusing
capacity and oxygen content of blood entering the pulmonary
artery (mixed venous blood). In particular, the greater the
imbalance of ventilation-perfusion ratios the more PaO2 tends to
differ from the calculated PAO2. (The difference between PAO2
and PaO2 is commonly referred to as the 'A-a gradient.'
However, 'gradient' is a misnomer since the difference is not due
to any diffusion gradient, but instead to V-Q imbalance and/or
right to left shunting of blood past ventilating alveoli. Hence 'A-
a O2 difference' is the more appropriate term.)
b) The alveolar-arterial PO2 difference, notated P(A-a)O2,
varies normally with age and FIO2. Up to middle age, breathing
ambient air, normal P(A-a)O2 ranges between 5 and 20 mm Hg.
Breathing an FIO2 of 1.0 the normal P(A-a)O2 ranges up to about
110 mm Hg23(Figure 2). If P(A-a)O2 is increased above normal
there is a defect of gas transfer within the lungs; this defect is
almost always due to V-Q imbalance.
This young woman's PaO2 was initially judged 'normal'
and so an abnormality in oxygen transfer was missed. The
calculated PIO2 and PAO2 were 147 mm Hg and 110 mm Hg,
respectively. Her P(A-a)O2 was elevated at 27 mm Hg (110 minus
83), indicating a state of V-Q imbalance, and therefore some
parenchymal lung disease or abnormality. Indeed, she returned
the next day with similar complaints, at which time a lung scan
showed defects interpreted as high probability for pulmonary
embolism.
c) Because of several assumptions in clinical use of the
alveolar gas equation, precision in calculating PAO2 is not
achievable.22 Fortunately an estimate of
P(A-a) O2 is usually sufficient for clinical purposes. In Case 3,
for example, the fact that the patient was hyperventilating and
PaO2 was only 83 mm Hg indicates an elevated P(A-a)O2 and
therefore a defect in gas exchange. The alveolar gas equation
shows that with hyperventilation PaO2 should go up; PaO2 should
be much higher than 83 mm Hg in a hyperventilating 27-year-old
patient. Similarly, a patient breathing 40% oxygen whose PaO2
and PaCO2 are normal for room air (e.g., PaO2 90 mm Hg,
PaCO2 40 mm Hg) has an elevated P(A-a)O2 and therefore a defect
in gas exchange; with this FIO2, PAO2 should be over 200 mm Hg
and PaO2 well over 100 mm Hg. These observations require
nothing more than knowledge of the alveolar gas equation and
simple mental calculation.
d) Since oxygen enters the pulmonary capillary blood by
passive diffusion, it follows that in a steady state the alveolar PO2
must always be higher than the arterial PO2. This fact is useful to
spot 'garbage' blood gas data, a not infrequent problem. For
example, a PaO2 of 150 mm Hg in a patient breathing 'room air'
at sea level (FIO2 = .21) must represent some kind of error, since
at all conceivable PaCO2 values the P(A-a)O2 would have a
negative value; even with extreme hyperventilation (PaCO2 10 mm
Hg) the alveolar PO2 would be no higher than 140 mm Hg. A
moment's reflection will reveal several possible explanations for
the apparently negative alveolar-arterial PO2 difference: the
patient was in fact breathing supplemental oxygen during or just
prior to the sample drawing; an air bubble in the arterial sample
syringe; a quality control or reporting error from the lab; a
transcription error - someone wrote down the wrong number; etc.
What about the oxygen values mentioned at the beginning of this
section? A PaO2 of 28 mm Hg would be normal on the summit of Mt.
Everest for a climber breathing ambient air. At the summit barometric
pressure is 253 mm Hg, which provides a PIO2 of only 43 mm Hg24
(Table V).
If the climber maintained PaCO2 at 40 mm Hg his PAO2 would be
minus 5 mm Hg, a value wholly incompatible with life! Ability to
oxygenate blood at this altitude without supplemental oxygen is made
possible (in large part) by extreme hyperventilation. On one expedition
to the summit, 10 minutes after supplemental oxygen was removed a
climber's end-tidal PCO2 (equivalent to PACO2) was measured at 7.5 mm
Hg; assuming an R value of 0.85, the PAO2 was only 35 mm Hg.24 Based
on a theoretical alveolar-arterial PO2 difference of 7 mm Hg, the
climber's PaO2 at the summit was estimated at 28 mm Hg - very low but
'normal' under the circumstances.24
A PaO2 of 55 mm Hg would likewise be normal at Pike's Peak,
Colorado, assuming a PaCO2 of 30 mm Hg from modest hyperventilation
and a P(A-a)O2 of 7 mm Hg (Table V). On the other hand, a PaO2 of 95
mm Hg would represent a serious abnormality in anyone breathing 100%
oxygen near sea level, as under these conditions PaO Forward any comments to:
based on PaO 2 alone, without reference to the
calculated PAO2.
CASE 3. A 27-year-old young woman came to the
emergency room complaining of pleuritic chest pain of
several hours duration. She was not a smoker but gave a
history of using birth control pills. Her chest x-ray and
physical exam were normal except for splinting with deep
inspirations. Arterial blood gas showed pH 7.45, PaCO2
31 mm Hg, HCO3- 21 mEq/L, PaO2 83 mm Hg (breathing
ambient air; PB 747 mm Hg). She was presumptively
diagnosed as having pleurodynia and discharged with pain
medication.
*All pressures in mm Hg; Pike's Peak and Mt. Everest data from summits
LOCATION
ALT.
PB
FIO2
PIO2
PaCo2
PAO2
PaO2
Sea Level
0
760
.21
150
40
102
95
Cleveland
500
747
.21
147
40
99
92
Denver
5280
640
.21
125
34
84
77
*Pikes's Peak
14114
450
.21
85
30
62
55
*Mt. Everest
29028
253
.21
43
7.5
35
28
ALT. = altitude in feet
PB = barometric pressure
FIO2 = fraction of inspired oxygen
PIO2 = pressure of inspired oxygen in the trachea
PaCO2 = arterial PCO2, assumed to = alveolar PCO2
PAO2 = alveolar PO2, PAO2 is calculated using an assumed R value of 0.8 except for the summit of Mt. Everest, where 0.85 is used 24
PaO2 = arterial PO2, assuming a P(A-a)O2 of 7 mm Hg at each altitude; each PaO2 value is normal for its respectove altitude
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