The effects of increased environmental pressure upon the body can be considered as: (i) effects on the gas-containing spaces; (ii) effects of the increased partial pressure of the respiratory gases; (iii) direct effects on cells and molecular mechanisms; (iv) consequences of the uptake by the blood and tissues of dissolved respiratory gases. As well as the effects of pressure itself, there are other complications at great depths, such as thermal imbalance. There are also some long term effects of diving, of which the precise causes are less certain.
Early divingThe breath-hold diver was certainly the first to venture below the surface, and divers who have no external source of gas to breathe underwater are at work today around the world, mostly gathering shellfish. During descent they hold their breath and at the same time must equalize the pressure in their middle ears via the eustachian tubes to avoid rupture of the ear-drum.
The compression of the air within the chest means also that, for a diver with full lungs who is just buoyant at the surface, descent reduces chest volume and makes his buoyancy progressively negative: he will not spontaneously float to the surface.
Similar effects are experienced by recreational breath-hold divers; they may also use a snorkel to allow breathing when on the surface. The duration of a breath-hold dive is determined by the rise of carbon dioxide in the lungs and blood, and hence the need and the stimulus to return to the surface for a breath of fresh air. Thus a diver may be tempted to prolong underwater duration by prior hyperventilation in order to wash out as much carbon dioxide as possible. This poses an additional hazard because hyperventilation reduces the carbon dioxide, but does not increase the oxygen, in the blood. The dive is prolonged because the carbon dioxide level remains tolerable for longer, but towards the end the oxygen has diminished significantly. A diminished blood content of oxygen at depth is at increased pressure and so may be sufficient to sustain consciousness but, during the inevitable return to the surface, the partial pressure of that oxygen diminishes and the breath-holder may lapse into unconsciousness — a potentially lethal situation.
The first attempts to remain underwater longer than breath holding allows may have included the use of hollow reeds as breathing tubes for concealment in battle, but many of the early drawings of submerged men breathing through long tubes to the surface are physically impossible because of the compression which would be imposed upon the chest by hydrostatic pressure.
The invention of the diving bell reputedly allowed Alexander the Great to descend to depth, but duration would have been limited by build up of carbon dioxide in the trapped air within. The bell used in the river Thames in 1691 by Edmund Halley, the Astronomer Royal, was replenished by barrels of air lowered down to it. When a reliable force pump was invented in 1788, those who ventured underwater could for the first time get sufficient compressed air, with the result that entirely new medical and physiological problems emerged. These were noticed first among men in new industrial applications: tunnelling below water and working in caissons.
Development of compressed air divingSimply pumping air down a hose may seem a crude technique, but it is still used today by many native fishermen. They hold the open end of a hose between the teeth and wear simple goggles. Such fisherman have a high incidence of crippling decompression illness (see below), but this is due not so much to the equipment as to lack of knowledge and training, since it occurs even when they are provided with modern underwater breathing apparatus.
A hose leading into a bucket inverted over the head, with a window, provides the simplest example of an early diving helmet and is similar to equipment being used today by attendants in large marine aquaria. One advantage is that gas is supplied for breathing at exactly the pressure of the depth of the helmet. The development in the early nineteenth century of the copper helmet attached to a closed dry suit made this system commercially viable.
Prolonged durations became practical but brought with them a greater risk of bubble formation in the tissues on return to atmospheric pressure. Joint pains after surfacing were considered by compressed air workers to be just routine. During the salvage of the Royal George off Spithead in 1843 the first case of neurological decompression illness in a diver was reported.
Problems associated with the exchange of respiratory gases at depth also became apparent and the work of John Haldane and others in the early twentieth century showed the importance of avoiding a build up of carbon dioxide. The greater the depth, the greater the volume of air that had to be pumped to the diver: at record depths of greater than 90 m, teams of 12 or more attendants were needed to man the pumps.
There was concern that divers at such depths sometimes behaved irresponsibly; it was not until 1934 that Al Behnke showed that this was due to the increased partial pressure of nitrogen. The so-called inert gas was acting like alcohol, an anaesthetic, or any narcotic.
The substitution of oxy-helium for compressed air was first demonstrated to be practical by Max Nohl in 1938, with a dive in the Great Lakes of the US. In the 1960s it was recognized that, due to the direct cellular effects of pressure during rapid compression to depths greater than 100 m, a number of manifestations occurred which became known collectively as the High Pressure Nervous Syndrome (HPNS) (see later).
Breathing apparatusThe design and use of underwater breathing apparatus (uba) presents its own problems. A complex closed-circuit rebreather apparatus was designed by Henry Fleuss in 1878. The diver breathed from a bag of pure oxygen (a ‘counter-lung’), which he topped up with more oxygen ‘as required’. His exhaled air was returned to the bag through a ‘scrubber’ which chemically removed the carbon dioxide. This is a hazardous procedure but nevertheless the apparatus was used successfully for the salvage of the flooded Severn Railway Tunnel. Because no bubbles emerge it was further developed for use in clandestine military operations in World War II — leading to recognition of the problems of acute oxygen neurotoxicity. Within strict depth limits it has also been useful for photographers and biologists.
Semi-closed-circuit uba is similar but uses an oxygen-nitrogen mixture rather than pure oxygen, enabling a greater depth to be achieved than with closed-circuit uba; the gas is supplied at a constant mass flow rate, which means that some bubbles emerge. This type of apparatus was developed as acoustically safe for those highly trained men whose underwater task was the clearance of enemy mines, but has recently been adopted by recreational divers. They require special training to minimize the risks from hazards peculiar to such apparatus: ‘dilution hypoxia’, ‘shallow water blackout’, and ‘soda-lime cocktail’.
Enjoyment of recreational diving depends on a sense of freedom in the water and, in particular, freedom from the encumbrance of helmets and hoses. This was made available to the world in the mid twentieth century by the development by Cousteau and Gagnan of a ‘demand regulator’. This allows just the right volume of gas, at the correct pressure for the diver's depth at that moment, to be delivered to the diver's mouthpiece from a tank of compressed air which he carries. Though not the first demand valve to be invented, it was the first to be adopted almost universally, and it is used widely for air and mixed gas diving by recreational and professional divers. Other types of uba with lower resistance have been developed to reduce the work of breathing at greater depths as gas density increases.
In the 1970s the need to exploit offshore oil and gas reserves led to the adoption of ‘saturation diving’ which had been pioneered by George Bond of the US Navy. The commercial diver avoids daily and prolonged decompressions from great depths by living at the surface in a chamber with an internal pressure similar to that of the worksite, until the task has been completed. Each day he descends by means of a pressurized diving bell to his work and, at the end of an in-water shift of several hours, returns to the deck chamber in the closed bell.
The gas-containing spaces and barotrauma
Aural barotraumaUnless additional gas can be admitted through the eustachian tube into the middle ear cavity during descent, to compensate for the reduction of gas volume there, the developing pressure differential may lead to injury — ‘barotrauma’. At depths as shallow as 3 m transudation and possible haemorrhage into the middle ear cavity, and ultimately an implosion of the ear-drum, can occur. The sudden influx of cold water into the middle ear is an abnormal stimulus to the labyrinth of the inner ear, and can cause total disorientation. Most divers avoid such trouble by learning to ‘clear their ears’ from the moment they leave the surface by using a simple swallowing technique. Even lesser degrees of aural barotrauma, perhaps if only one ear is ‘sticky’, can lead to underwater disorientation; this can become a hazard, especially as immersion also reduces sensations from limbs and joints, and as visibility may be impaired.
There is a risk of infection to a middle ear exposed by barotrauma. Even worse, attempts to ‘clear’ the ears by forcing gas through the eustachian tube too vigorously can raise the cerebrospinal fluid pressure enough to rupture a membrane which separates the middle from the inner ear, causing permanent damage to hearing and balance.
Pulmonary barotraumaIn contrast to the middle ear, which is damaged predominantly during the compression phase, the lungs are at risk during ascent: when the diver has inhaled gas at a pressure greater than atmospheric, this gas will expand progressively as he approaches the surface, and failure to breathe out the expanding gases can lead to pulmonary barotrauma — probably the commonest cause of death among sports divers. (The breath-hold diver should not be affected by this, since during ascent his lungs are merely re-expanding to their original volume.) Clearly the risk of lung damage is greatest if the diver holds his breath during ascent — yet lung rupture can occur even when he has exhaled continuously and even when it is known that he has no abnormality in his chest which might impede the venting of gas; rapid expiration may itself tend to collapse the small airways, trapping gas in the lungs.
Rupture allows gas to escape from the lungs into the pleural cavities (pneumothorax) or into the lung blood vessels (gas embolism) — a serious form of ‘decompression illness’.
Barotrauma due to equipmentcan arise when there is a gas-containing space which becomes rapidly smaller with increasing pressure, if there is no adequate inflow to maintain the volume. An unanticipated rapid fall through the water by a traditional helmeted diver whose helmet pressure is controlled at the surface can lead to a fatal ‘chest squeeze’. A squeeze of the half mask of a scuba diver, if not equalized by small exhalations through the nose during descent, can damage the eyes by conjunctival oedema and haemorrhage. Even a dry suit, worn for thermal protection, can lead to painful pinches of the skin if compression of the air within it is uncompensated.
Increased partial pressure of respiratory gasesWhen the total pressure is increased, the partial pressure of each component gas in the inspired air (or other mixture) is increased proportionately; these increased pressures in the lungs equilibrate with the blood, resulting in greater ‘tensions’ of the gases in solution in body fluids.
Oxygen neurotoxicityOxygen can cause an epileptiform fit, but only when breathed at pressures greater than that of pure oxygen at normal atmospheric pressure (∼100 kPa). A partial pressure of 150 kPa in oxy-nitrogen mixtures is an acceptable upper limit for short-term use, but military divers rebreathing pure oxygen for swimming use a limit of 176 kPa which occurs at 7.6 m. The threshold for oxygen toxicity varies greatly between and even within individuals and from day to day, and is influenced by the amount of physical work being done. For a diver at rest, requiring oxygen treatment, up to 280 kPa is commonly used. Intermittent oxygen breathing, with 5 min air breaks every 20 min or so, reduces the risk of oxygen toxicity.
Characteristically the diver has no warning of an impending fit. Occasionally there is an impression of hearing the sound of an engine within the head, but this comes too late for the diver to avoid a convulsion. If this occurs in the water, especially when wearing some kinds of uba, it is likely to be fatal; those using a helmet or with some other guaranteed airway are less likely to drown.
Oxygen pulmonary toxicityIn contrast to neurotoxicity the ill-effects of prolonged oxygen breathing on the lung are relatively slow in onset. Characteristic first signs are a dry cough with chest pain; vital capacity shows a progressive impairment which at first is reversible. Later there may be pulmonary oedema which can become irreversible. These effects can usually be avoided by estimating and controlling the cumulative oxygen dose. With more prolonged exposures at lesser partial pressures (~30 kPa), there can be a slow diminution in the ability to transfer oxygen to the blood.
Nitrogen narcosisLike all ‘inert’ gases, nitrogen has actions on nerve cells like those of alcohol and some anaesthetics. At increasing nitrogen partial pressure (proportional to depth when breathing air) the diver becomes incapable of behaving responsibly and this can have disastrous effects upon in-water safety. For this reason amateur divers are recommended to stay shallower than 30 m and commercial divers are restricted to 50 m when breathing compressed air. Some amateur divers practise ‘extreme air diving’ and a number of potential record breakers have achieved 90 m — but not all have returned to the surface. Extreme air diving is really rather stupid.
Carbon dioxidemay build up in some types of breathing apparatus and create breathlessness and headaches. A number of divers have been shown to tolerate raised carbon dioxide: they do not respond to it, as normal persons, by increasing their breathing. While one might expect this to be a potentially useful adaptation, in fact the synergism of carbon dioxide with nitrogen and with raised partial pressures of oxygen is thought to be a cause of otherwise unexplained loss of consciousness. ‘Carbon dioxide retainers’ may therefore be at a greater risk of an underwater accident than others.
The direct effects of pressureThe High Pressure Nervous Syndrome (HPNS) begins in the compression phase of deep diving when oxy-helium is used to avoid nitrogen narcosis. It is worse with rapid compression rates and increases with depth. The neurological manifestations include tremors, nausea, and vomiting, and there are changes in the electroencephalogram. Helium itself has no significant narcotic effects at depths to around 600 m and it has been shown that the HPNS is not a gas effect. It is thought to be due to the direct effects of pressure upon transmission of nerve impulses. Paradoxically the HPNS can be ameliorated by the addition of a narcotizing agent, and 5% nitrogen is the one most readily available for oxy-helium divers. Such ‘trimix’ dives have been shown to be an effective solution for very deep diving, but are not used commercially for reasons of expense related to the difficulties of gas recovery and purification; rather, a very slow staged compression rate is used to avoid HPNS in oxy-helium diving, developed over years of experience.
Uptake of gases into solution in the bodyNitrogen accounts for 80% of air breathed into the lungs, so is at 80% of the total gas pressure, but it is relatively insoluble in the blood so that body tissues at sea level contain very little. At depth, breathing air, progressively more nitrogen slowly dissolves in blood and in all body tissues. The amount that accumulates depends on both the depth and the duration of the dive. Then, when rising to the surface, nitrogen is released, and can cause decompression sickness (including ‘the bends’) if the rise is too rapid.
Long-term health effectsThe only known long term hazard of diving is aseptic necrosis of bone (dysbaric osteonecrosis), a disintegration in the substance of the head, neck, and shaft of the long bones, where it causes problems very rarely, or under the cartilage in the shoulder and hip joints, where it can be painful and crippling. It can occur even after only a single exposure to raised environmental pressure and has a latency of months or years before symptoms arise. Cases among sports and European commercial divers are rare, but the condition is prevalent in shell-fishing divers who tend to be unaware of safe decompression procedures.
Much has been said about the possible long-term damage to the central nervous system caused by diving, but when sequelae from known episodes of neurological decompression illness are excluded, the evidence is not dramatic. There may be some pathological changes but there is little or no evidence that these are harmful.
In conclusionThose who dive must be mentally, medically, and physically fit to do so. Some obvious contraindications are epilepsy and cardiac inadequacies, while those who are diabetic or paraplegic should dive only under the careful restrictions of an appropriate organization. Lung and other diseases require assessment of fitness to dive by a doctor experienced in this environment. Assessment is not easy but is justified not only by the subsequent avoidance of unnecessary diving accidents but also for the safety of those who otherwise might suddenly become rescuers.
Those who wish to dive should do so only after rigorous training and each must recognize that the most important feature of every subsequent dive plan is to include the recognition, assessment, and control of risk. Diving is hazardous and the sea is an unforgiving environment.
Bennett, P. B. and and Elliott, D. H. (1993). The physiology and medicine of diving, (4th edn) Saunders, London.
Bove, A. A. (1997). Bove and Davis diving medicine, (3rd edn). Saunders, Philadelphia.
Edmonds, C.,, Lowry, C.,, and and Pennefather, J. (1994). Diving and subaquatic medicine, (3rd edn). Butterworth-Heinemann, London.
Undersea Medical Society (1983). Key documents of the biomedical aspects of deep-sea diving selected from the world's literature, 1608–1982. Undersea Medical Society Bethesda, Maryland.
See also decompression sickness; gases in the body; hyperbaric chamber; nitrogen; oxygen.
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