AIDA Funded Lung-Squeeze Study, Preliminary Results Published
Since the death of Nicholas Mevoli in 2013, the Freediving community has been searching for ways to accurately predict a Freediver’s risk of significant injury during competition, and in particular, their risk of pulmonary barotrauma, the scientific term for ‘lung squeeze’. Swedish Professor of Environmental Physiology, Erika Schagatay is one of the foremost (and only) scientists publishing rigorous research into the physiology of Freediving and in 2014 AIDA commissioned her to investigate the validity of measuring arterial oxygen saturation as a useful ‘dry-land’ marker of these injuries. The preliminary results of that study are now available and make for some interesting reading. As always, our physiology stalwart Dr Otter, takes a look:
Note:- If you’re new to freediving physiology you might want to take a look at some of Dr Otter’s Physiology Bootcamp articles to get you started, as there’s some technical information in the article that follows.
Lung-Squeeze Research so Far
One of the first things that strikes me as most useful about this study is that it provides an overview (which scientists call a “literature review”) of what is already known about lung squeeze. It’s not comprehensive but it makes the important point that whilst it might seem like lung squeeze should happen on all dives below 30 or 40m, in fact trained freedivers routinely dive below even 100m (the deepest, of course being 214m) without any appreciable injury at all. Why should this be?
The simple fact is that nobody knows, but it now seems reasonably clear that it doesn’t just depend on genetics. Training, preparation and technique all play important roles. As Erika puts it:
“there appears to be considerable plasticity and potential to alter human lung function and mechanics by directed training methods and exposure to extreme environments rather than evolutionary traits that limit deep diving.”
In short, deep freediving can be seen as a safe and natural activity for most humans, without the expectation of serious injury. If you’re regularly getting squeezed, particularly at shallow depths, the chances are that you’re doing something wrong.
This is an important point. One of the 2 major factors that were identified as contributing to Nick Mevoli’s death was “repeated barotrauma close in time before the lethal event”. It now seems reasonably clear that small lung injuries which are not given time to heal, can add up in the end to make a large, life-threatening injury more likely. This is the major driving force behind recent attempts (of which this study is one major example) to identify ways to accurately predict which divers have a) already suffered an injury and b) are likely to suffer one in the future. Currently the approach has been to use physiological markers like arterial oxygen saturation (SaO2) as a proxy for lung injury and to exclude these divers from further competition. As we’ve previously identified, however, until now it hasn’t been clear how good a marker post-dive SaO2 might be for actual lung injury.
Methods Used to Test Post-Dive SaO2 as a Marker for Lung Squeeze
(Full article available here:) submitted_preliminary_aida_sao2_summary.pdf
Erika and her team sampled a total of around 100 divers after competition dives to between 25 and 100m, measuring their arterial oxygen saturation using a pulse oximeter for 10 minutes after surfacing. As well as recording the amount of time it took for their saturations to normalise, they asked divers to report on their symptoms (breathlessness, coughing, wheeze, feeling of discomfort, etc) and did some ultrasound scans of the diver’s lungs to identify “Ultrasonic Lung Comets” (ULCs - not anywhere near as exciting as they sound!) which are markers of pulmonary oedema - that is, abnormal fluid in the lungs.
They analysed the data in 2 different ways:
- They worked out the time it takes for ‘normal’ uninjured divers’ saturations to return to normal. They did this by excluding any divers who reported symptoms and measuring the time it took for the saturation monitor to register above 97% .
- They then looked at the association between the other markers of injury (reported symptoms and findings of ULCs on ultrasound) and a low SaO2 after the SaO2 ‘should’ have normalised. They had 2 thresholds for defining “low” SaO2, a stricter threshold - below 97% - and a less strict threshold - below 95%.
Research Findings - the Link Between Low Oxygen Saturations and Lung Injury
The first and most important finding in this study is that almost all of the symptom-free (“normal”) divers had normal saturations within 10 minutes after surfacing. Of the divers that didn’t, 83% had some kind of symptom when the less strict SaO2 cutoff (<95%)was used and 57% with the stricter (<97%) cutoff. Looking at ultrasound images of the lungs (albeit with smaller numbers of divers) also showed a strong association between O2 saturations and the presence of visible markers of lung injury (ULCs). Divers with larger numbers of ULCs had significantly lower O2 Saturations 10mins after surfacing.
Putting it simply, if you’ve got saturations of less than 95% 10 minutes after a dive, the chances are you have some kind of lung injury. If your saturations are less than 97% but greater than 95%, it’s still more likely than not that you have an injury, but there’s also a fair chance (about 43%) that you don’t.
A word of caution about this, though: there were a few divers who did have symptoms who nevertheless still had normal O2 saturations 10mins after surfacing. This means that just because your saturations are normal, it doesn’t mean that you definitely don’t have an injury. Symptoms, it seems, are always the best guide. In addition to this, the ultrasound data suggested that even in cases where lung injury was obvious, saturations all returned to normal within an hour after surfacing, so delayed testing is unlikely to be of benefit.
Second, there was good evidence that deeper dives (even normal, symptom-free ones) take longer to recover from than shallower ones. In a few individual cases, dives below 100m resulted in low O2 saturations up to 12min after surfacing, even in the absence of symptoms. To me, this implies that at least some of the oedema that’s been observed in previous studies of lung-squeeze may be ‘physiological’, that is, related to the normal adaptation of well-trained lungs to deep diving.
Third, Blackout, by itself, did not seem to affect the oxygen saturations at 10 minutes after surfacing. Where divers recovered from a blackout and still had low SaO2 at 10mins after surfacing, they also tended to have symptoms of lung injury. To me this suggests that a) SaO2 is not an appropriate way of measuring the risk of future divers to a diver who’s suffered a blackout and b) Blackout and Lung-Squeeze should be treated as completely separate issues. New and different research is required to identify ways of measuring an athletes risk of serious injury on dives following a blackout.
Tune in next week for more in-depth discussion about this research and its implications for competition safety.