Latent hypoxia is a condition where the oxygen content of the lungs and arterial blood is sufficient to maintain consciousness at a raised ambient pressure, but not when the pressure is reduced to normal atmospheric pressure. It usually occurs when a diver at depth has a lung gas and blood oxygen concentration that is sufficient to support consciousness at the pressure at that depth, but would be insufficient at surface pressure. This problem is associated with freediving blackout and the presence of hypoxic breathing gas mixtures in underwater breathing apparatus, particularly in diving rebreathers.
The term latent hypoxia strictly refers to the situation while the potential victim is at depth, still conscious, and not yet hypoxic, but is also loosely applied to the consequential blackout, which is a form of hypoxic blackout also referred to as blackout of ascent or deep water blackout, though deep water blackout is also used to refer to the final stage of nitrogen narcosis.
The minimum tissue and vascular partial pressure of oxygen which will maintain consciousness is about 20mmHg. This is equivalent to approximately 30mmHg in the lungs. Approximately 46 ml/min oxygen is required for brain function. This equates to a minimum arterial oxygen partial pressure (PaO2) of 29mmHg at 868 ml/min cerebral flow.
An ascent blackout, or deep water blackout, is a loss of consciousness caused by cerebral hypoxia on ascending from a deep freedive (breath-hold dive), typically of ten metres or more when the swimmer does not necessarily experience an urgent need to breathe and has no other obvious medical condition that might have caused it, or from a dive using underwater breathing apparatus while using a breathing gas which has too low an oxygen fraction to support consciousness at the surface. Breath-hold victims typically black out close to the surface, sometimes even as they break surface, and have been seen to approach the surface without apparent distress only to sink away. Breath-hold victims are usually established practitioners of deep breath-hold diving, are fit, strong swimmers and have not experienced problems before. Blackout by this mechanism may occur even after surfacing from depth and breathing has commenced if the inhaled oxygen has not yet reached the brain and may be referred to as a surface blackout. Divers ascending using breathing apparatus typically ascend at slower ascent rates to avoid decompression sickness, and the depth at which consciousness is lost tends to follow the oxygen partial pressure of the breathing gas.
The partial pressure of oxygen in the air or other breathing gas mixture in the lungs controls the oxygen loading of blood. A critical PO2 of 30mmHg in the lungs will sustain consciousness when breathing is resumed after a breath-hold dive. This is about 4% oxygen in the lungs and 45% oxygen saturation of the arterial blood. At 30 msw (4 bar), 2% by volume oxygen in the lung gas gives a PO2 of 60mmHg. At 10 msw (2 bar), for the same 2% oxygen, the PO2 would be 30mmHg, i.e. marginal. At the surface the same 2% oxygen drops to 15mmHg, ignoring metabolic use.
See also: Asphyxia. The usual consequence, if the airway is not protected, is drowning. A breath-hold diver who has blacked out and has been promptly returned to the surface, will usually regain consciousness within seconds. While the diver is still unconscious underwater, they are at high risk of drowning. While unconscious the diver has lost voluntary bodily control, but still has protective reflexes that protect the airway. One of these is laryngospasm, which closes the larynx, to preventing water from entering the lungs. If the diver has reached the surface, and the divers face is kept above water, when the laryngospasm relaxes spontaneous breathing will often resume. The laryngospasm will eventually relax, and if the diver is still underwater then water will enter the airway and may reach the lungs which will cause complications if resuscitation is successful, and secondary drowning is possible. The time between loss of consciousness and death varies considerably depending on a number of factors but can be as little as two and a half minutes.
If the diver's airway is protected by a full-face mask or diving helmet, the immediate risk is death by asphyxiation, which can occur within a few minutes of cessation of breathing. If the diver sinks and the pressure increases sufficiently, the gas may become capable of supporting consciousness again, but the problem of latent hypoxia remains until a higher oxygen content gas is provided. If the diver is on surface supply, a prompt switch of gases may be sufficient to restore consciousness, and this may also apply to a scuba diver if immediate and appropriate action is taken by another diver. Immediate surfacing of a hypoxic diver using underwater breathing apparatus presents the risk of decompression illness from lung barotrauma or decompression sickness, and the risk depends on the pressure exposure history of the diver.
Risk of latent hypoxia leading to blackout and further complications depends on the mode of diving in use.
The diver who has lost consciousness due to latent hypoxia is already hypoxic, and should be brought to the surface as soon as possible, while protecting the airway. There are no contraindications to immediate surfacing for a breath-hold diver, and the mouth and nose may be blocked to prevent involuntary aspiration of water.
The first priority is ventilation at the earliest possible opportunity, and in many cases this may be sufficient. If ventilation with sufficient oxygenation is achieved promptly, and there has been no aspiration of water it is quite possible that no further treatment will be needed. If there is a delay the prognosis deteriorates rapidly. CPR may be necessary. Aspiration of water may require hospitalisation for observation, and if necessary, treatment for complications due to water in the lungs. Treatment is generally as for drowning. Supplementary oxygen is generally recommended.