Pulse oximetry
An old
saying goes: The lack of oxygen not only
stops the machinery, it wrecks it. Hypoxia of the brain first causes
confusion, then coma, and eventually irreversible brain damage. Other organs
follow that pattern, even though most can survive hypoxia longer than the
brain. Thus, knowing whether arterial blood carries oxy-gen to the organs
assumes great importance. Because oxyhemoglobin is red and reduced hemoglobin
bluish, this color difference can be exploited to assess the oxygenation of
blood. Clinically, we recognize cyanosis, but we cannot well grade the degree of
bluishness.
Enter
pulse oximetry. The concept is what you might call “elegant.” A probe sends
light impulses into a finger (or earlobe or nose or toe) and then collects the
light that has passed through the tissue. The light comprises two wavelengths:
one (infra-red) more likely to be absorbed by oxyhemoglobin, the other (red) by
reduced hemoglobin. By rapidly (too rapid for the eye to recognize) alternating
the two wavelengths with no light at all, the unit is able to estimate the
proportion of oxyhemoglobin to reduced hemoglobin. This is called “functional
saturation.” Some instruments estimate (not
measure) the other species of hemoglobin in blood (methemoglobin,
carboxyhemoglobin) and compare the oxyhemoglobin as a percentage of the sum of
all known hemoglobins. This is called “fractional saturation,” which will be a
little lower than functional saturation.
We want
to know the percentage of oxyhemoglobin saturation in arterial blood (rather
than in the tissue or in arterial plus venous blood), therefore we need to
catch the saturation reading in the artery, rather than in the whole finger. To
accomplish this, the unit functions as a plethysmograph assessing the thickness
of the finger (or earlobe or nose or toe). Because the tissue swells a little
with each arterial pulsation, the unit can discard data arising during diastole
and report on data only recorded during systole, which represent arterial
blood. The saturation is reported as SpO2,
the p referring to the fact that the
measurement is based on pulse oximetry rather than on a direct in vitro measurement of oxygen
saturation from an arterial blood
sample, which would be SaO2.
A healthy person breathing room air at sea level (at least not at Mount
Everest) should have an SpO2 of about 98% +/− 2%. Here is a rough correlation of SpO2to
arterial partial pressure of oxygen(PaO2):
SpO2 : PaO2
100% : 100 mmHg or higher
90% : 60 mmHg
60% : 30 mmHg
In patients with normal lungs and nothing more than a small
physiologic shunt (2% to 4%), the PaO2 should be within spitting
range of inspired oxygen pressure. If it is substantially different, a shunt is
likely to exist.
There is more to pulse oximetry than outlined here. But we will not
dwell on issues of other dyes interfering with the measurements, on the amount
of pulsa-tion required, on the influence of venous pulsation, or on the
confounding effects of external light. For all of these issues, we refer you to
one of many exhaustive texts on monitoring or pulse oximetry.
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