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Shallow water blackout
A shallow water blackout is a loss of consciousness caused by cerebral hypoxia towards the end of a breath-hold dive in water typically shallower than five metres (16 feet), when the swimmer does not necessarily experience an urgent need to breathe and has no other obvious medical condition that might have caused it. Victims are often established practitioners of breath-hold diving, are fit, strong swimmers, and have not experienced problems before.
Many drowning and near drowning events occur among swimmers who black out underwater while free-diving or doing breath-hold pool laps. Blacking out, or browning out, near the end of a breath-hold dive is common. Although the mechanism is well understood, it is not common knowledge among breath-hold divers.
Shallow water blackout is related to, but differs from deep water blackout in its characteristics, mechanism and prevention; deep water blackout is precipitated by depressurisation on ascent from depth. Blackout may also be referred to as a syncope or fainting.
The role of hyperventilation
Otherwise unexplained blackouts underwater have been associated with the practice of hyperventilation. Survivors of shallow water blackouts often report using hyperventilation as a technique to increase the time they can spend underwater. Hyperventilation, or over-breathing, involves breathing faster and deeper than the body naturally demands and is often used by divers in the mistaken belief that this will increase oxygen (O2) saturation. Although this appears true intuitively, the breathing rate dictated by the body alone is sufficient, even during quite strenuous activity, to ensure that the body is saturated with as much O2 as is necessary. What is really happening differs from divers' understanding; these divers are extending their dive by closing down the body's natural breathing mechanism, not by increasing oxygen load. The mechanism is as follows:
The primary urge to breathe is triggered by high carbon dioxide (CO2) levels in the bloodstream. Oxygen levels in the body are able to be detected, but the level of carbon dioxide in the blood is the primary determinant of respiratory drive. Persistently elevated levels of carbon dioxide in the blood (hypercapnia) can cause the body to become desensitized to hypercapnia, in which case the body relies on oxygen levels in the blood to maintain respiratory drive. This is illustrated in the scenario of type II respiratory failure in which persistently elevated blood carbon dioxide levels become tolerated by the body and hypoxia is responsible for maintaining respiratory drive. However, in a normal healthy person, hyperventilation causing low blood carbon dioxide levels (hypocapnia) will reduce respiratory drive and leave the person susceptible to loss of consciousness due to hypoxia. The first sign of low O2 is a brownout or unconsciousness. In this situation, there is no bodily sensation that warns a diver of an impending blackout. Rising CO2 levels in the bloodstream are what cause a reflexive urge for breathing. Because CO2 builds up in the bloodstream when O2 is metabolized, the CO2 needs to be expelled. However, the body can detect CO2 levels accurately and it relies on this to control breathing. The CO2 level guides breathing, therefore depleting CO2 too fast by hyperventilating leads to hypocapnia. The result is unconsciousness with little warning. Significantly, victims drown quietly underwater without alerting anyone to the fact that there is a problem and are typically found on the bottom as shown in the image right. Pool lifesavers are trained to scan the bottom for the situation shown.
The diagram below shows the O2 and CO2 levels in the blood over the duration of a safe dive. Prior to the dive the green area shows the stabilisation of O2 and CO2 through normal breathing. The dive ends safely when the diver is forced to the surface by an urgent need to breathe.
In the next diagram hyperventilation prior to the dive has artificially depressed CO2 levels without elevating the O2 level. This pre-dive state is hence likely to result in shallow water blackout. Now note how the O2 level drops into the diver's blackout zone before the CO2 can rise enough to force the diver to resurface to breathe. The dive is extended a little, but this diver may not survive.
Breath-hold divers who hyperventilate before a dive are at risk of drowning. Many drownings unattributed to any other cause result from shallow water blackout and could be avoided if this mechanism were properly understood and the practice eliminated. Hyperventilation does not increase diving time by any notable amount. Shallow water blackout can be avoided by ensuring that carbon dioxide levels in the body are properly calibrated prior to diving and that appropriate safety measures are in place; this can be achieved if divers do the following:
Shallow water blackout should be considered alongside deep water blackout.
Deep water blackout
The mechanism for deep water blackout differs from that for shallow water blackouts and does not necessarily follow hyperventilation. However, hyperventilation will exacerbate it and the two should be considered together. Shallow water blackouts can happen in extremely shallow water; brownouts can be induced even on dry land following hyperventilation and apnoea. However, the effect becomes much more dangerous in the ascent stage of a deep free dive. Refer to deep water blackout for more detail. There is considerable confusion surrounding the terms shallow and deep water blackout and they are made to refer to different things, or used interchangeably, in different water sports circles. For the purposes of this article the two are separate phenomena with the following characteristics:
Deep water blackout occurs as the surface is approached following a breathe-hold dive of over ten metres and typically involves deep, free-divers practicing dynamic apnoea depth diving usually at sea. The immediate cause of deep water blackout is the rapid drop in the partial pressure of oxygen in the lungs on ascent.
Shallow water blackout only occurs where all phases of the dive have taken place in shallow water where depressurisation is not a factor and typically involves dynamic apnoea distance swimmers, usually in a swimming pool. The primary mechanism for shallow water blackout is hypocapnia brought about by hyperventilation prior to the dive.
|This article is licensed under the GNU Free Documentation License. It uses material from the Wikipedia article "Shallow_water_blackout". A list of authors is available in Wikipedia.|