I analyzed Audrey’s dive back in 2011 using a computer simulation of lung mechanics and alveolar collapse (reference 1) and pulmonary gas exchange (reference 2). The depth profile was obtained from Kim McCoy’s data recorder that Audrey wore. I didn’t comment on this analysis at the time out of sensitivity to the tragedy. But results of the simulation provide insight into what happened.
What is unique about her dive is not just the record depth, but the long time spent at or near the maximum depth while she struggled and waited for assistance. It was 2 min and 8 sec from sled contact at 170 m to blackout at 120 m. If we assume her lung volume TLC plus packing was 8 litres at the start, collapse depth predicted by the simulation would be somewhere around 180 m. We can assume her lungs were not completely collapsed at her maximum depth of 170 m, but the excessive time spent there resulted in additional gas absorption and further decrease of lung volume. This is because O2 is still taken up from the lungs, but CO2 does not flow into the lungs at depth because its high solubility retains it in the blood until near the surface when alveolar CO2 drops enough to reverse the gradient and allow CO2 back into the alveoli. So it is conceivable that her lungs collapsed while she was stuck near bottom depth, and this ultimately caused blackout from hypoxia. This is what I called the “hypoxia wall”, which is predicted to occur after total lung collapse. I discussed this idea a little more in a recent review paper (reference 3).
When I ran her dive profile through the simulation, I found that at the time of blackout her lungs would have collapsed completely, at which point arterial PaO2 drops to 25.4 mmHg, which is exactly when the blackout threshold should occur. Blackout typically occurs around 20 to 30 mmHg, depending on various factors. You might think that the high ambient pressure would keep PaO2 high at depth, but arterial oxygen drops to the level of venous oxygen PvO2 due to full shunting of blood past the collapsed alveoli, which shuts off pulmonary gas exchange. Predicted arterial PaCO2 was 57.3 mmHg at blackout - not an extreme level, but similar to that seen when terminating static apnea.
Hypoxia is therefore the primary cause of blackout, not high CO2. Once there is loss of consciousness, the negative airway pressure at that depth due to outward rib cage recoil and relaxation of the closed glottis would cause water to be forced into the lungs.
1. Fitz-Clarke JR. Lung compression effects on gas exchange in human breath-hold diving. Respir Physiol Neurobiol 165: 221-228, 2009.
2. Fitz-Clarke JR. Mechanics of airway and alveolar collapse in human breath-hold diving. Respir Physiol Neurobiol 159: 202-210, 2007.
3. Fitz-Clarke JR. Breath-hold diving. Compr Physiol 8: 585-630, 2018.