Freediving blackout


Freediving blackout, breath-hold blackout, or apnea blackout is a class of hypoxic blackout, a loss of consciousness caused by cerebral hypoxia towards the end of a breath-hold dive, when the swimmer does not necessarily experience an urgent need to breathe and has no other obvious medical condition that might have caused it. It can be provoked by hyperventilating just before a dive, or as a consequence of the pressure reduction on ascent, or a combination of these. Victims are often established practitioners of breath-hold diving, are fit, strong swimmers and have not experienced problems before. Blackout may also be referred to as a syncope or fainting.
Divers and swimmers who black out or grey out underwater during a dive will usually drown unless rescued and resuscitated within a short time. Freediving blackout has a high fatality rate, and mostly involves males younger than 40 years, but is generally avoidable. Risk cannot be quantified, but is clearly increased by any level of hyperventilation.
Freediving blackout can occur on any dive profile: at constant depth, on an ascent from depth, or at the surface following ascent from depth and may be described by a number of terms depending on the dive profile and depth at which consciousness is lost. Blackout during a shallow dive differs from blackout during ascent from a deep dive in that blackout during ascent is precipitated by depressurisation on ascent from depth while blackout in consistently shallow water is a consequence of hypocapnia following hyperventilation.

Terminology

Different types of freediving blackout have become known under a variety of names; these include:
In this article constant pressure blackout and shallow water blackout refers to blackouts in shallow water following hyperventilation and ascent blackout and deep water blackout refers to blackout on ascent from depth. Some free divers consider blackout on ascent to be a special condition or subset of shallow water blackout but the primary underlying mechanisms differ. This confusion is exacerbated by the fact that in the case of blackout on ascent, hyperventilation induced hypocapnia also may be a contributory factor even if depressurisation on ascent is the actual precipitator.
Some scuba diving curricula may apply the terms shallow-water blackout and deep-water blackout differently; deep-water blackout being applied to the final stage of nitrogen narcosis while shallow water blackout may be applied to a blackout from a deep free dive. Nitrogen narcosis does not normally apply to freediving as free-divers start and finish the dive with only a single lungful of air and it has long been assumed that free divers are not exposed to the necessary pressure for long enough to absorb sufficient nitrogen. Where these terms are used in this manner there is usually little or no discussion of the phenomenon of blackouts not involving depressurisation and the cause may be variously attributed to either depressurisation or hypocapnia or both. This problem may stem from the origin of the term latent hypoxia in the context of a string of fatal, shallow water accidents with early military, closed-circuit rebreather apparatus prior to the development of effective oxygen partial pressure measurement. In the very different context of dynamic apnea sports careful consideration of terms is needed to avoid potentially dangerous confusion between two phenomena that actually have different characteristics, mechanisms and prevention measures. The application of the term shallow water blackout to deep dives and its subsequent association with extreme sports has tended to mislead many practitioners of static apnea and dynamic apnea distance diving into thinking that it does not apply to them even though isobaric shallow water blackout kills swimmers every year, often in shallow swimming pools.
The CDC has identified a consistent set of voluntary behaviors associated with unintentional drowning, known as dangerous underwater breath-holding behaviors; these are intentional hyperventilation, static apnea, and hypoxic training.
Other terms generally associated with freediving blackout include:

Mechanisms

The minimum tissue and venous partial pressure of oxygen which will maintain consciousness is about. This is equivalent to approximately in the lungs. Approximately 46 ml/min oxygen is required for brain function. This equates to a minimum arterial ppO2 of at 868 ml/min cerebral flow.
Hyperventilation depletes the blood of carbon dioxide, which causes respiratory alkylosis, and causes a leftward shift in the oxygen–hemoglobin dissociation curve. This results in a lower venous partial pressure of oxygen, which worsens hypoxia. A normally ventilated breath-hold usually breaks with over 90% saturation which is far from hypoxia. Hypoxia produces a respiratory drive but not as strong as the hypercapnic respiratory drive. This has been studied in altitude medicine, where hypoxia occurs without hypercapnia due to the low ambient pressure. The balance between the hypercapnic and hypoxic respiratory drives has genetic variability and can be modified by hypoxic training. These variations imply that predictive risk cannot be reliably estimated, but pre-dive hyperventilation carries definite risks.
There are three different mechanisms behind blackouts in freediving:
  1. Duration-induced hypoxia occurs when the breath is held long enough for metabolic activity to reduce the oxygen partial pressure sufficiently to cause loss of consciousness. This is accelerated by exertion, which uses oxygen faster or hyperventilation, which reduces the carbon dioxide level in the blood which in turn may:
  2. * increase the oxygen-haemoglobin affinity thus reducing availability of oxygen to brain tissue towards the end of the dive,
  3. * suppress the urge to breathe, making it easier to hold the breath to the point of blackout. This can happen at any depth.
  4. Ischaemic hypoxia is caused by reduced blood flow to the brain arising from cerebral vasoconstriction brought on by low carbon dioxide following hyperventilation, or increased pressure on the heart as a consequence of which can reduce blood circulation in general, or both. If the brain used more oxygen than is available in the blood supply, the cerebral oxygen partial pressure may drop below the level required to sustain consciousness. This type of blackout is likely to occur early in the dive.
  5. Ascent-induced hypoxia is caused by a drop in oxygen partial pressure as ambient pressure is reduced on ascent. The oxygen partial pressure at depth, under pressure, may be sufficient to maintain consciousness but only at that depth and not at the reduced pressures in the shallower waters above or at the surface.
The mechanism for blackout on ascent differs from hyperventilation induced hypocapnia expedited blackouts and does not necessarily follow hyperventilation. However, hyperventilation will exacerbate the risk and there is no clear line between them. Shallow water blackouts can happen in extremely shallow water, even on dry land following hyperventilation and apnoea but the effect becomes much more dangerous in the ascent stage of a deep freedive. There is considerable confusion surrounding the terms shallow and deep water blackout and they have been used to refer to different things, or be used interchangeably, in different water sports circles. For example, the term shallow water blackout has been used to describe blackout on ascent because the blackout usually occurs when the diver ascends to a shallow depth. For the purposes of this article there are two separate phenomena Shallow water blackout and Blackout on ascent as follows:

Shallow water blackout

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/or deeper than the body naturally demands and is often used by divers in the mistaken belief that this will increase oxygen saturation. Although this appears true intuitively, under normal circumstances the breathing rate dictated by the body alone already leads to 98–99% oxygen saturation of the arterial blood and the effect of over-breathing on the oxygen intake is minor. What is really happening differs from divers' understanding; these divers are extending their dive by postponing the body's natural breathing mechanism, not by increasing oxygen load. The mechanism is as follows:
The primary urge to breathe is triggered by rising carbon dioxide levels in the bloodstream. Carbon dioxide builds up in the bloodstream when oxygen is metabolized and it needs to be expelled as a waste product. The body detects carbon dioxide levels very accurately and relies on this as the primary trigger to control breathing. Hyperventilation artificially depletes the resting concentration of carbon dioxide causing a low blood carbon dioxide condition called hypocapnia. Hypocapnia reduces the reflexive respiratory drive, allowing the delay of breathing and leaving the diver susceptible to loss of consciousness from hypoxia. For most healthy people, the first sign of low oxygen levels is a greyout or unconsciousness: there is no bodily sensation that warns a diver of an impending blackout.
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 staged image above. Survivors of shallow water blackout are typically puzzled as to why they blacked out. Pool life guards are trained to scan the bottom for the situation shown.
Breath-hold divers who hyperventilate before a dive increase their risk of drowning. Many drownings unattributed to any other cause result from shallow water blackout and could be avoided if this mechanism was properly understood and the practice eliminated. Shallow water blackout can be avoided by ensuring that carbon dioxide levels in the body are normally balanced prior to diving and that appropriate safety measures are in place.
A high level of hypocapnia is readily identifiable as it causes dizziness and tingling of the fingers. These extreme symptoms are caused by the increase of blood pH following the reduction of carbon dioxide, which acts to lower the pH of the blood. The absence of any symptoms of hypocapnia is not an indication that the diver's carbon dioxide is within safe limits and cannot be taken as an indication that it is therefore safe to dive. Conservative breath-hold divers who hyperventilate but stop doing so before the onset of these symptoms are likely to be already hypocapnic without knowing it.
Note that the urge to breathe is triggered by rising carbon dioxide levels in the blood and not by the reduction of oxygen. The body can actually detect low levels of oxygen but this is not normally perceptible prior to blackout. Persistently elevated levels of carbon dioxide in the blood, hypercapnia, tend to desensitise the body to carbon dioxide, in which case the body may come to rely on the oxygen level in the blood to maintain respiratory drive. This is illustrated in the scenario of type II respiratory failure. However, in a normal healthy person there is no subjective awareness of low oxygen levels.