Interpretation of arterial oxygen tension
Oxygenation of arterial blood is generally assessed by measurement of arterial
oxygen tension from arterial blood gases, or by noninvasive measurement of
oxygen saturation using pulse oximetry. This card will discuss interpretation
of arterial oxygen tension, while the use of pulse oximetry is reviewed
separately. (
See
"Pulse oximetry"). Other related topics discussed elsewhere
include general issues regarding to arterial blood gas measurement (
See
"Measurement of arterial blood gases") and interpretation of
acid-base status from arterial blood gases. (
See
"Simple and mixed acid-base disorders").
Oxygenation of blood is achieved by passive diffusion of oxygen from the
alveolus to the pulmonary capillary. The majority of oxygen uptake by
pulmonary capillary blood occurs via binding to hemoglobin within red blood
cells, whereas only a small amount is dissolved in plasma. The arterial oxygen
tension reflects the end result of this transport process, and can be affected
by several physiologic disturbances.
INDICATORS OF OXYGENATION — Assessing the
efficiency of oxygenation requires knowledge of the inspired oxygen
concentration and the partial pressures of oxygen (PaO2) and carbon dioxide
(PaCO2) in arterial blood. The alveolar-arterial oxygen gradient is often used
for this purpose, and is determined by subtracting the arterial oxygen tension
from the calculated alveolar oxygen tension. The most common form of the
alveolar gas equation, which is used to calculate the alveolar oxygen
concentration, is:
PAO2 = (FiO2 x [Patm - PH2O])
- (PaCO2 ÷ R)
where PAO2 = alveolar oxygen tension in mmHg; FiO2 = fractional inspired
oxygen concentration; Patm = atmospheric pressure in mmHg; PH2O = partial
pressure of water (47 mmHg at 37 degrees C); and R = respiratory quotient
(approximately 0.8 at steady state, depending upon the relative utilization of
carbohydrate, protein, and fat).
This equation is a simplification of the actual derived relationship between
FiO2, PaCO2, and PaO2 and may deviate up to 10 mmHg (when FiO2 = 1.0) from the
more rigorous, full calculation. In addition, values used in the equation may
not be precisely known, particularly the FiO2 (unless on room air) and the
value of R. The alveolar-arterial oxygen gradient (A-a gradient) is obtained
by subtracting the measured arterial oxygen tension from the calculated
alveolar tension. The normal A-a gradient varies with age and ranges from
seven to 14 mmHg when breathing room air. An equation which can be used to
estimate the expected A-a gradient is [
1]:
A-a gradient = 2.5 + 0.21 x age in years
With higher inspired oxygen concentrations, the A-a gradient also increases.
In one series the A-a gradient when breathing 100 percent oxygen varied from 8
to 82 mmHg in patients less than 40 years of age and from 3 to 120 mmHg in
patients greater than 40 years of age [
2].
Two other useful indices of oxygenation include [
3,4,5]:
• The ratio of arterial oxygen tension to
calculated alveolar oxygen tension (PaO2 ÷ PAO2). The
lower limit of normal of (PaO2 ÷ PAO2) is 0.77-0.82 [
3].
This ratio is commonly used in the critical care arena to approximate the
change in PaO2 which will occur when the FIO2 is changed, and when used for
this purpose is most reliable when less than 0.55.
• The ratio of arterial oxygen tension to FiO2
(PaO2 ÷ FiO2). The normal value for (PaO2 ÷ FIO2) is
300 to 500, with a value <250 indicative of a clinically significant gas
exchange derangement.
The (PaO2 ÷ PAO2) may better reflect gas exchange over
a broader range of FiO2, but because of the simplicity of calculation, the
(PaO2 ÷ FiO2) is often used clinically.
MECHANISMS OF HYPOXEMIA — Pathophysiologic
mechanisms leading to hypoxemia include hypoventilation, ventilation-perfusion
mismatch, right-to-left shunting, diffusion impairment, and reduced inspired
oxygen tension.
Hypoventilation — Hypoventilation leads to
an elevation in alveolar CO2 tension and a simultaneous reduction in alveolar
oxygen tension. The PAO2 is reduced according to the alveolar gas equation in
cases of pure hypoventilation, but the A-a gradient should be normal (although
prolonged hypoventilation may produce areas of atelectasis and an increase in
the A-a gradient [
6]).
For example, if R = 0.8, the PAO2 will fall 1.25 mmHg for each 1 mmHg increase
in PCO2. As apparent from the alveolar gas equation, the hypoxemia due to pure
hypoventilation can be corrected with a small increment in the concentration
of inspired oxygen.
Pure hypoventilation is seen in disease states which cause central nervous
system depression (drug overdose, structural or ischemic CNS lesions involving
the respiratory center), disorders of neural conduction (amyotrophic lateral
sclerosis, Guillain-Barré syndrome, high cervical spine injury), disorders
causing muscular weakness (polymyositis, muscular dystrophy), and diseases of
the chest wall (flail chest, kyphoscoliosis). (
See
"Control of ventilation").
Ventilation-perfusion mismatch —
Ventilation-perfusion (V/Q) abnormalities due to regional imbalances in the
relationship between blood flow and ventilation commonly lead to hypoxemia.
Although the alveolar gas equation can be used to model the lung as a whole,
it cannot be used to predict regional alveolar gas content, since the
respiratory exchange ratio is not constant.
The gas composition of lung regions is determined by the relative magnitudes
of ventilation and perfusion.
• Lung regions which have low ventilation
compared to perfusion will have a low alveolar oxygen content and high CO2
content.
• Lung regions with high ventilation compared to
perfusion will have a low CO2 content and high oxygen content.
The V/Q ratio varies with position in the normal lung, being lower in basilar
than in apical regions. It is the summation of this "normal" V/Q
heterogeneity that accounts, in part, for the normal A-a gradient.
Diseases which alter regional V/Q relationships and can therefore cause
hypoxemia include obstructive lung diseases, pulmonary vascular diseases, and
parenchymal diseases. Hypoxemia from V/Q mismatch can usually be corrected
with low to moderate flow supplemental oxygen.
Right to left shunt — Right-to-left
shunting can be viewed as an extreme example of V/Q mismatch, in which the V/Q
ratio is zero for certain lung regions. Clinically, parenchymal diseases
leading to atelectasis or alveolar flooding, including lobar pneumonia and
acute respiratory distress syndrome, may cause shunt physiology. Shunt may
also occur from pathologic vascular communications, such as pulmonary
arteriovenous malformations or intracardiac right-to-left shunts. Hypoxemia
from shunt physiology does not correct as readily with oxygen as does
hypoxemia from V/Q mismatch.
The magnitude of shunt can be approximated from the shunt equation:
Qs/Qt = (CcO2 - CaO2) ÷ (CcO2 - CvO2)
where Qs/Qt = shunt fraction; CcO2 = end-capillary oxygen content; CaO2 =
arterial oxygen content; and CvO2 = mixed venous oxygen content
CaO2 and CvO2 can be obtained by blood gas measurement of arterial and mixed
venous blood, respectively. CcO2 is determined by using the alveolar gas
equation to calculate alveolar oxygen tension, and then assuming that full
equilibration occurs between alveolar gas and pulmonary capillary blood.
Diffusion impairment — Diffusion impairment
occurs when the available path for movement of oxygen from from alveolus to
capillary is altered. It can contribute to hypoxemia by reducing the
efficiency of gas transfer. Diffuse fibrotic diseases are the classic entities
in which diffusion abnormalities occur. However, the magnitude of the
contribution to hypoxemia is controversial, since these diseases also commonly
lead to severe V/Q mismatch.
The contribution of diffusion impairment to hypoxemia is thought to be minimal
at rest, even in interstitial lung disease. However, diffusion impairment is
believed to contribute significantly to hypoxemia induced by exercise in
interstitial lung disease. In exercise, the rate of pulmonary capillary blood
flow increases, and transit time through the pulmonary capillary circulation
decreases. When the decrease in transit time coupled with diffusion
impairment, there may be insufficient time for equilibration of oxygen
tensions in pulmonary capillary blood and alveolar gas.
Reduced inspired oxygen tension — Reduced
inspired oxygen tension directly affects alveolar oxygen tension through the
alveolar gas relationship. The most common clinical situation in which this is
important is high altitude.
OXYGEN DELIVERY — Delivery of oxygen to the
tissue beds is determined by the arterial oxygen content and the cardiac
output, as defined by the following relationship:
DO2 = 10 x CO x CaO2
where DO2 = oxygen delivery (mL O2/min); CO = cardiac output (L/min); CaO2 =
arterial oxygen content (mL O2/100 mL blood)
Oxygen delivery may therefore be impaired by multiple mechanisms, as shown in
Figure 1.
• For any arterial oxygen tension, the oxygen
content of the blood is affected by the level and the affinity state of
hemoglobin. As an example, patients with carbon monoxide poisoning will have a
reduction in arterial oxygen content despite a normal PaO2 and hemoglobin
concentration due to a reduction in available O2 binding sites on the
hemoglobin molecule.
• Reduced cardiac output states will lead to
impairment in tissue oxygen delivery. Tissue hypoxemia and lactic acidosis may
result, depending upon the severity of the impairment.
While the above processes affect oxygen delivery, the relationship between
global tissue oxygen delivery (as measured by DO2), global oxygen utilization,
and tissue oxygenation is complex [
7].
• Tissue hypoxia may occur despite adequate
oxygen delivery, as in cyanide poisoning. Cyanide interferes with oxygen
utilization by the cellular cytochrome system, leading to cellular hypoxia.
• In disease states such as sepsis, tissue
ischemia may occur despite normal or elevated values of DO2, possibly due to
diversion of blood flow away from vital organ beds. This has led to a number
of trials of "goal oriented" hemodynamic therapy in high-risk
surgical patients and critically ill medical patients, in whom DO2 is
augmented to supranormal goals. Although conflicting results make this a
controversial area, more recent data cast doubt on the utility of this
strategy (
show
table 1). In one trial, 762 critically ill patients were randomized to
control therapy, a high cardiac index (achieved by volume expansion, inotropic
agents, and vasodilators), or therapy aimed at normalization of the mixed
venous oxygen saturation [
8].
There were no differences among the three groups in mortality rates at
discharge from the intensive care unit or at six months.
