Deep Water Blackout - Possible Mechanisms For Deep Water Blackout

Possible Mechanisms For Deep Water Blackout

Three causes have been put forward, possibly acting simultaneously:

1. Voluntary suppression of breathing;
2. Rapid depressurisation;
3. Self-induced hypocapnia.

1. Voluntary suppression of breathing. Deep water blackout is sometimes attributed to the practiced diver’s ability through training to suppress the urge to breathe. If surviving divers are aware that they have heavily suppressed the urge to breathe towards the end of the dive there is a tendency to look no further for an explanation. However, there are two problems with this as an explanation:

• a). Even with a high level of training the urge to breathe is almost impossible to overcome; swimmers typically suffer an uncontrollable, violent, deep inhalation of water even when, intellectually, they know that to do so is fatal. In this case the drowned swimmer will be found with water deep in the alveoli of the lungs consistent with inhalation and is a simple case of running out of air and drowning. Victims of deep water blackout, if they have any water in the lungs at all will have a limited amount in the bronchi consistent with natural ingress after death.

• b). Victims of deep water blackout closely observed from both below and above water often do not exhibit the signs of distress associated with an uncontrollable urge to breathe and those that have survived a blackout often report no such distress. Many blackout events have been closely observed and even filmed because deep dynamic apnoea dives are a competitive event and very deep dives require a considerable support crew both above and below water. Anecdotal accounts of healthy divers holding their breath to the point of unconsciousness are difficult to substantiate and the ability, if it exists, is certainly extremely rare.

For these two reasons voluntary suppression of breathing might be considered a contributory factor in that it helps push other factors past the threshold limit but it is not the primary factor.

2. Rapid depressurisation. Because deep water blackout occurs as the diver approaches the surface without necessarily showing signs of distress, depressurisation is clearly implicated in the cause. Consciousness depends on a minimum partial pressure of oxygen in the brain not on the absolute quantity of the gas in the system. (See pulmonary alveolus for details of gas pressure in the lung.) At the surface, the air in the lungs is under 1 atmosphere of pressure; at 10 metres, the water pressure doubles the pressure of air in the lungs to 2 atmospheres. Recreational deep breath-hold dives can often go to 20 metres, competitive deep dives can go much deeper, and the current free-dive record exceeds 200 metres. Ten metres is easily achievable by a reasonably fit and competent swimmer. Most people go unconscious when the partial pressure of oxygen (ppO₂) in their lungs, normally 105 mmHg falls below ~30 mmHg. Ten metres of water effectively doubles this to 60 mmHg putting the diver above the blackout threshold until they hit the 30 mmHg limit on ascent. A ppO₂ of 45mmHg at ten metres will pretty much ensure a blackout between four metres and the surface. S.Miles termed this latent hypoxia. Although quite comfortable on the bottom the diver may actually be trapped and unaware that it is now no longer possible to ascend safely through the shallow layers above and a diver pushing the limits may expect to go unconscious without warning just as he or she approaches the surface. Rapid depressurisation certainly answers the question as to why victims black out so close to the surface and without distress but it is still unclear why it happens at all. A physiological explanation dependent on pressurisation of the body is required. Two theories have been put forward as to how this might work:

• a). Pressurisation delays the urge to breathe by interfering with the ability of the body's carotid body to detect CO₂ levels in the blood or its ability to act appropriately on what it does detect, the system being calibrated for sea level only. The body relies on the carotid body to accurately measure the build up of CO₂ in the blood to determine the trigger for the urge to breathe; it cannot detect a lack of oxygen prior to a syncope so anything that disrupts the process is dangerous. Although interesting this theory remains to be proved. Intuitively it might be supposed that increasing the partial pressure of CO₂ at depth would, if anything, bring forward the urge to breathe rather than delay it but in practice pressure would appear to have no effect on the urge to breathe. Furthermore, if pressure did delay the urge to breathe then the ascent itself should bring on this urge, this also does not seem to be the case and a characteristic of deep water blackout is that the urge is absent or not acute. At the moment this theory appears unconvincing.

• b). There is some discussion that the act of rapid depressurisation through at least one atmosphere when the body is close to but has not yet crossed the sea-level threshold level for cerebral hypoxia is enough in itself to cause syncope but this too remains unproven and the physiology unclear.

If neither of these theories can fully account for blackout it is necessary to seek another cause.

3. Self-induced hypocapnia. Hyperventilation leading to hypocapnia and subsequent loss of an appropriate urge to breathe is the mechanism behind shallow water blackout; refer to the shallow water blackout article for a detailed description of how this commonly misunderstood mechanism works. Many practitioners of deep water breath-hold diving use hyperventilation as a misguided method of extending the duration of their bottom time and so this mechanism is almost certainly relevant to deep water blackouts also. If the diver has hyperventilated, the mechanism is essentially that for shallow water blackout but hypoxia is delayed by pressure at depth and sets in only when the pressure drops to 1.25 to 1 atmospheres. This explains why divers who die like this do so very close to the surface on their way up and why they may not have felt any urgency to breathe at all; fit, free-divers ascending from deep dives can go unconscious without any warning.

In conclusion, depressurisation on ascent is an explanation for the consistent depth location of deep water blackouts but is currently an insufficient explanation of cause unless accompanied by an underlying suppression of the urge to breathe through self-induced hypocapnia via hyperventilation. Experienced free-divers are put at special risk by their practiced ability to suppress the carbon dioxide induced urge to breathe. Unfit and inexperienced swimmers rarely have the ability to descend deep enough to induce deep water blackouts and are unable to suppress the urge to break surface at the very onset of distress, if they drown it is much more likely to be from other causes. The strong and the fit are at most risk. Practitioners of deep breath-hold diving should be counselled on the role of depressurisation regarding the timing of deep water blackouts but should be given the same advice for dive preparation as suggested for shallow water blackout, which centres on relaxation and avoids hyperventilation. Where deep breath-hold divers are observed to use hyperventilation timely and informed advice may save their lives but experience suggests that divers are reluctant to change their practice unless they have a very clear understanding of the mechanics of the process.