Shallow water blackout
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
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 meters (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 depressurization on ascent from depth. Blackout may also be referred to as a syncope or fainting.
Pathophysiology
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. 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 stabilization 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:
- Take a moment on the edge of the water to relax and allow blood oxygen and carbon dioxide to reach equilibrium.
- Breathe absolutely normally; allow the body to dictate the rate of breathing to make sure the carbon dioxide levels are properly calibrated.
- If excited or anxious about the dive take extra care to remain calm and breathe naturally; adrenalin also causes hyperventilation without the diver knowing.
- When the urge to breathe comes on near the end of the dive immediately seek access to air.
- Never pre-ventilate using blended gas mixtures such as Nitrox, Trimix or Heliair that might purge carbon dioxide in a bid to extend the dive.
- Never dive alone. Dive in buddy pairs, one to observe, one to dive.
- Buddy pairs must both know cardiopulmonary resuscitation (CPR) current practice.
Shallow water blackout should be considered alongside deep water blackout.