The increases in ambient pressure to which a diver is exposed at various depths are summarized.
Various methods are used to supply air to the diver. With the simplest, e.g. a snorkel, the limiting factor, which occurs below 0.5 m, is the respiratory effort required to suck air into the lungs. At greater depths this ‘forced negative-pressure ventilation’ ultimately results in pulmonary capillary damage and haemorrhagic pulmonary oedema. Scuba tanks, the method commonly used for sporting diving down to 50 rn, carry compressed air at a pressure balanced with the water pressure.
Divers who work at great depths for commercial purposes or for underwater exploration breathe helium/oxygen or nitrogen/oxygen mixtures delivered by hose from the surface.
A wide variety of complex medical problems may affect divers at all depths. These are summarized below.
COMPRESSION (i.e. DESCENT)
Barotrauma of the middle ear (‘squeeze’) is the commonest disorder in divers. This is caused by an inability to equalize the pressure in the middle ear usually as a result of Eustachian tube blockage. Deafness occurs with eventual rupture of the tympanic membrane followed by acute vertigo.
Paranasal sinus barotrauma (‘squeeze’) is due to dysfunction of the nasal or paranasal sinus with blockage of the sinus ostea. Pain over the frontal sinus occurs. Treatment of both conditions is with decongestants. It can be prevented by avoiding diving when the airways are blocked, e.g. with a respiratory tract infection.
When compressed air is breathed below 30 m the narcotic effects of nitrogen cause impairment of cerebral function with changes of mood and performance that may be lifethreatening. The condition reverses rapidly on ascent. Nitrogen narcosis is avoided by replacing air with helium/oxygen mixtures, which can enable divers to descend to 700 m.
At these great depths neurological disturbances occur that are believed to be the result of the direct effects of pressure on neurones. Tremor, hemiparesis and psychological changes may occur.
Pure oxygen cannot be used for diving because oxygen becomes toxic to the lungs when the alveolar oxygen pressure exceeds 1.5 atmospheres absolute (5 m of water) and to the nervous system at around 10 m of water. In the lungs, linear atelectasis appears and there is endothelial cell damage with exudation and pulmonary oedema. In the nervous system there is initially a feeling of apprehension, nausea and sweating, followed by muscle twitching and generalized convulsions, which may be fatal underwater.
DECOMPRESSION (i.e. ASCENT)
Decompression sickness (‘the bends’) occurs on returning to the surface and is caused by the release of inert gases, usually nitrogen or helium, which form bubbles in the tissues as the ambient pressure falls. It only occurs when the diver ascends too rapidly. Decompression tables are available for calculating the time needed to come to the surface safely from any given depth.
This can take a mild form (type 1 ‘non-neurological bends’), with skin irritation, mottling or joint pain only, or be more serious (type 2 ‘bends’), in which a variety of neurological features appear. Patients with type 2 ‘bends’ may develop cortical blindness, hemiparesis, sensory disturbances or cord lesions. If nitrogen bubbles occur in the pulmonary vessels, divers experience retrosternal discomfort, dyspnoea and cough (‘the chokes’). These symptoms develop within minutes or hours of a dive.
Treatment is with oxygen. In addition, all but the mildest forms of decompression sickness (i.e. skin mottling alone) require recompression, usually in a pressure chamber.
A long-term problem is aseptic necrosis caused by infarction due to nitrogen bubbles lodging in nutrient arteries supplying bone. It is seen in 5% of deep-sea divers. Neurological damage may also persist. Lung rupture, pneumothorax and surgical emphysema These emergencies occur principally when divers ‘breathhold’ while making emergency ascents after losing their gas supply. Following lung rupture the patient notes severe dyspnoea, cough and haemoptysis. Pneumothorax and emphysema usually respond to 100% oxygen. Air embolism may occur and should be treated with recompression and hyperbaric oxygen.