Hypoxia and Breath-Hold Diving

In a simple breath-hold, with no immersion or preceding hyperventilation, the breaking point (the irresistible urge to breathe) is initiated mainly by a rise in CO2 level, and to a lesser extent by a fall in arterial O2.

In breath-hold diving, hypoxic blackout is sometimes called breath-hold syncope or shallow water blackout. Because ‘shallow water blackout’ was first used in 1944 to describe loss of consciousness from the use of closed-circuit diving suits, it is best avoided in the breath-holding context. ‘Hypoxic blackout’ is a reasonable alternative.

There are two causes of this disorder – hyperventilation and ascent – and because they may occur concurrently, they are often confused. The hyperventilation effect is independent of depth and may be encountered in 1-meter-deep swimming pools, often by children trying to swim greater distances underwater.

Breath-hold divers who train to extend their breath-hold and also dive deep (e.g. free diving competitors, spear fishing) risk hypoxia of ascent, with loss of consciousness and subsequent drowning.

With hypoxia there is little or no warning of impending unconsciousness. With increased experience the breath-hold diver can delay the need to inhale by various techniques, without improving the O2 status. Breath-hold time can be extended (but not with increased safety) by, for example, feet-first descent, training (adaptation), swallowing, inhaling against a closed glottis and diaphragmatic contractions.

One way of avoiding this hypoxia is to inhale 100 per cent O2 before the breath-hold.


In 1961, Craig observed that swimmers who hyperventilated could stay longer underwater but then lose consciousness with little or no warning1. They were often competing, against others or themselves, and often exercising. The hyperventilation extended their breath-holding time because it washed out a large amount of CO2 from the lungs, often to half the normal levels.

The build-up of CO2 is the main stimulus forcing the swimmer to surface and breathe. After hyperventilating it takes much longer for this level (the ‘breaking point’) to be reached. Under these conditions, the diver may extend the breath-hold to the point that PaO2 drops to a level inadequate to sustain consciousness. Increased exercise exacerbates this effect by increasing O2 consumption.

The combination of these two effects (hyperventilation and exercise) can be deadly. One can demonstrate this dangerous combination in the following experiment: When the swimmer is concentrating on some purposeful goal, such as trying to spear a fish or retrieve a catch, he or she is more likely to ignore the physiological warning symptoms of an urge to breathe (resulting from the rise in CO2 level in the blood) and delay the breaking point.

The dangers of hyperventilation and breath-hold diving are diagrammatically illustrated in Figure 16.3. It illustrates that, with earlier hyperventilation, the time to reach the irresistible urge to breathe (the breaking point) is prolonged. This extra time may allow the PaO2 to fall to dangerous levels (hypoxic danger zone).

A diagrammatic representation of changes in arterial oxygen and carbon dioxide levels with breath-holding.
Figure 16.3 A diagrammatic representation of changes in arterial oxygen and carbon dioxide levels with breath-holding. Point A, without preceding hyperventilation; point B, with preceding hyperventilation. PaCO2, arterial partial pressure of carbon dioxide; PaO2, arterial partial pressure of oxygen.


Ascent hypoxia was first described in military divers losing consciousness as they surfaced with low O2 levels in their rebreathing equipment.

In breath-hold divers, with descent the pressure rises proportionately in the alveolar gases, thus increasing the available O2, CO2 and nitrogen. Some O2 can be absorbed and used, some CO2 absorbed and buffered, and some nitrogen absorbed and deposited in tissues.

Thus, if a diver having 100 mm Hg O2 and 40 mm Hg CO2 in the alveolar gases was immediately transported to 2 ATA, the lungs would halve their volume; the O2 would be 200 mm Hg, and the CO2 80 mm Hg. Both would pass into the pulmonary capillary blood, the O2 to be used and the CO2 to be buffered. The alveolar PO2 and PCO2 therefore would decrease rapidly. By the time these values were both back to ‘normal’ levels, with O2 at 100 mm Hg and CO2 at 40 mm Hg, the diver would appear to be in a satisfactory respiratory status – until he or she ascended. With an expansion of the lungs to twice their size at depth, the pressures in both gases would halve; i.e. the O2 would drop to 50 mm Hg (approaching a potentially dangerous hypoxia level) and the CO2 to 20 mm Hg – if the ascent was immediate.

Because ascents do take time, more O2 will be consumed, extracted from the lungs during the ascent, and the CO2 will increase toward normal as a result of the gradient between the pulmonary blood and alveoli.

The drop in O2 is then able to produce the loss of consciousness, the ‘syncope’ or ‘blackout’, commonly noted among spear fishers. This condition is referred to as hypoxia of ascent. In deeper dives it becomes more likely, and with some very deep dives, the loss of consciousness may occur on the way to the surface in the top 10 metres (probably an explanation for the ‘7-metre syncope’ described by French workers).

Other causes of hypoxia in breath-hold diving include salt water aspiration and the drowning syndromes (see Chapters 21, 22 and 24).