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.