I guess I
showed my obsolescence with the observation about welder’s oxygen, as one
person on the list stated, “they were different twenty years ago”, I didn’t
realize the spec’s had changed.
However,
over-reliance on finger pulse oximetry is something that pilot’s need to
understand. The reason is that pulse oximetry measures O2 saturation in
peripheral blood, which may be different from cerebral oxygen saturation, and
may lag behind.
For more info
read the article below which appeared on our international AME list.
More than a few docs on the list are professors or research docs. They
essentially all agree with the concepts.
Bob
Mitchell
L-320
Senior AME
At the Airlines Medical
Directors Association scientific meeting in
Orlando in 2006, Professor John Ernsting
presented a joint paper with Group Captain David Gradwell summarising the
theoretical and experimental results of the effect of hyperventilation on
arterial oxygen saturation.
They concluded that the
limitations of pulse oximetry in hypoxia should be widely recognised in
aviation. Here are the reasons.
Reduction of alveolar PCO2
(partial pressure CO2)
to 20 mmHg when breathing air at 14k raises arterial SO2 (oxygen Saturation) to
96%, which is produced in the absence of hyperventilation by breathing air at
1,500
feet.
A degree of
hyperventilation is the normal response to acute exposure of breathing air at
or above 8,000
feet.
Using the relationship
between arterial PCO2, arterial SO2 and jugular venous PO2 (partial pressure oxygen),
it can be calculated that when air is breathed at altitudes above 10k,
arterial oxygen saturation is a very poor indicator of
minimum
PO2 in the brain if the
individual is hyperventilating. This also applies when oxygen-air gas mixtures
are breathed to avoid significant hypoxia at altitude. This is because
hyperventilation is known to have a very large effect on arterial SO2 in
hypoxia, which is not matched by the cerebral
SO2.
Professor Ernsing's and
David Gradwell's paper confirmed this theoretical calculation by experimental
study. The results showed that hyperventilation which reduced the end-tidal
PCO2 produced large increases in arterial SO2 which was not matched by
increases in cerebral SO2.
The take-home message,
which we should share with our high-flying general aviation colleagues, can be
summarised thus:
1) Hyperventilation is a
normal response to any degree of hypoxia.
2) This hyperventilation
affects the peripheral arterial oxygen
saturation.
3) The result is that a
pulse oximeter can give misleading information about the saturation of oxygen
in the cerbral circulation. Unfortunately, it is not 'fail-safe' because the
pulse oximeter may provide reassurance about satisfactory arterial SO2 when in
fact the brain is hypoxic.
4) Pulse oximetry is a
useful tool, but its limitations in aviation must be recognised. Ideally, an
oxygen-enriched gas should be breathed whenever flying above a cabin altitude
of 10,000feet.