en.wikipedia.org/wiki/Freediving_blackout#Shallow_water_blackout

Otherwise unexplained blackouts underwater have been associated with the practice of hyperventilation.[2][3][4][25] 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.[10] The mechanism is as follows:

The primary urge to breathe is triggered by rising carbon dioxide (CO2) levels in the bloodstream.[25] 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.[25] 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.[10]

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.[citation needed]

The diagram above shows the O2 and CO2 levels (partial pressures) in the blood over the duration of a safe dive. Stabilisation of O2 and CO2 levels through normal breathing are shown on the left. The dive ends safely when the diver is forced to the surface by an urgent need to breathe.

In the diagram above hyperventilation prior to the dive has artificially depressed CO2 levels (partial pressures) without elevating the O2 level. This pre-dive state is likely to result in shallow water blackout. 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 length is extended but the diver may not survive.
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.[1][5]

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 (alkalosis) 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.[12]

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.[10] Persistently elevated levels of carbon dioxide in the blood, hypercapnia (the opposite to hypocapnia), 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.[12]