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  • AutorenbildMichael Mutter

HRV and decompression stress

Can a decompression model be derived from Heart Rate Variability (HRV)?

Picture: courtesy Patrick Rhyner, Tauchschule H2O

I recently read with great interest in the DAN newsletter the discussion of a study on HRV (heart rate variability) and decompression-induced physiological stress.

What is it about?

Decompression leads to physiological stress. The cause is assumed to be the formation of inert gas bubbles, which trigger decompression illness (DCI) via gas emboli or direct effects on the tissues. Today it is known that inflammatory processes are also involved in the development of decompression sickness. HRV is easy to measure with an ECG and is an established parameter to assess heart health. HRV is smaller the sicker the heart and vice versa. However, this relationship does not only apply to the heart, but to the organism as a whole. Put simply, HRV decreases the sicker a person becomes. Now, many diseases are associated with inflammation, including decompression illness. Therefore, a correlation between decompression stress, HRV and inflammation would be expected.

The study

Schirato et al. tested this hypothesis. 28 divers were subjected to 2 dives each (with at least 48h surface interval). ECGs were recorded before and after each dive and inflammatory markers were determined in the blood. Indeed, there was a correlation between HRV, inflammatory markers and decompression stress. Specifically, the more inflammatory markers increased and the greater the decompression stress, the more HRV decreased. In the DAN article, the discussant speculates that in the future we could determine decompression obligation based on our HRV by having dive computers record our heart rate similar to a smart watch on the wrist.

Surrogate markers should not be equated with clinically manifest disease.

Unfortunately, the only diver who developed decompression sickness in this study showed an inverse behavior of HRV. The HRV did not decrease (as it should have been expected from the above mentioned correlations), but increased. Of all things, the correlation with the inflammation markers and the decompression stress was not correct.


Thus, the idea of being able to deduce the risk of decompression sickness from the heart rate recorded on the wrist belongs to the realm of science fiction. And it is shown once again that surrogate markers should not be equated with clinically manifest disease.

That is why the clinical approach chosen by Keller and Bühlmann in their decompression research is still fascinating today, in which "only" manifest decompression illnes counted. It is precisely this that interests me as a physician in a preventive measure: whether someone gets sick or not. Whether, as in the case of decompression stress, bubbles or inflammation markers occur or other values are favorably influenced in the case of illness is of secondary interest. The only thing that counts is whether (decompression) illness is prevented or not.

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