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Diving Physiology |
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Diving Physiology |
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1. Introduction
3. Barotrauma
4. Pulmonary Overinflation Syndromes
5. Indirect Effects of Pressure
One of the fascinations of diving is that we are entering an environment which we can normally only enter for short amounts of time or, at deeper depths, not at all. Our body is simply not designed to stay underwater for more than short periods of time. With SCUBA humans have designed the means to overcome these limitations. The fact however remains, that by entering an environment that cannot sustain us we are faced with numerous risks of which we should be aware so that we can take the necessary precautions to avoid harm. This page will detail some of these hazards and what should be done to avoid them.
Some respiratory problems divers can encounter occur due to the pressures at depth others can occur at any time but are exacerbated at depth.
This is an abnormal deficiency of oxygen in the arterial blood, depriving body tissues of the oxygen they need for their normal functioning. The risk of this happening on SCUBA, other than through a loss of the air supply, is minimal. This problem is more relevant when diving with gas mixes or rebreathers due to low oxygen partial pressures. I will therefore not go into this further for the time being.
Carbon Dioxide Toxicity (hypercapnia)
This is an abnormally high level of carbon dioxide in the body tissues. Once again this problem is more relevant to hard hat diving and rebreathers. In SCUBA diving this problem can occur through improper breathing techniques, for example skip breathing when a diver tries to conserve his air supply by reducing his breathing rate. Symptoms of hypercapnia are confusion, inability to concentrate, drowsiness, loss of consciousness and convulsions. An increase in the partial pressure of carbon dioxide can be noticed by monitoring one's breathing rate. Both a shortness of breath as well as hyperventilation can be indicative for this problem. Hypercapnia is treated by relieving the excess partial pressure of carbon dioxide through ascension and proper ventilation.
When breathed, carbon monoxide will displace oxygen from hemoglobin which reduces the amount of oxygen the blood can transport to the tissues causing hypoxia. Since fresh air does not contain significant amounts of carbon monoxide, a contamination of a diver's breathing supply usually only occurs if the air intake of a compressor is too close to the exhaust of an internal combustion engine. Carbon monoxide concentrations of 0.002 ata (atmospheres) can be fatal. The symptoms of carbon monoxide poisoning are almost identical to those of hypoxia and include lack of concentration, lack of muscle control, weakness, dizziness and confusion. If the carbon monoxide concentration is high enough unconsciousness can occur without the victim noticing these warning signs. Carbon monoxide poisoning requires medical attention. First aid measures include getting the victim to fresh air and if available administering oxygen. Carbon monoxide poisoning can be prevented by ensuring that the compressor is in good mechanical condition and that its air intake is located away from engine exhausts. When obtaining tanks or air from dive shops it is a good idea to take a look at their compressor (i.e. location and condition) and to taste the air in your scuba tank before diving. Even though carbon monoxide is odorless and tasteless the other pollutants in exhaust fumes are noticeable. If the air tastes oily or bad don't dive with it.
Barotrauma occurs due to the reaction of air filled body spaces to hydrostatic pressure. There are two types of Barotraumas:
1. Squeezes: These injuries happen on descent when the hydrostatic pressure exceeds the pressure found in the air filled body space, forcing the surrounding tissue into the space in an attempt to create equilibrium.
2. Reverse squeezes: These injuries happen on ascent when the pressure found inside the air filled body space exceeds the hydrostatic pressure and cannot escape. The air then forces the tissues apart causing injuries.
This is the most common type of barotrauma. The anatomy of the ear can be viewed by clicking here. The eardrum completely seals off the outer ear canal from the middle ear space. On descent, water pressure increases on the external surface of the eardrum and must be counterbalanced by an increase of air pressure on its inner surface. This is accomplished by the passage of air through the eustachian tube which connects the middle ear space with the nasal passages. A barotrauma can occur if this tube is blocked and the pressure difference cannot be equalized. Blockage is usually caused by mucous. The symptoms are sharp pain caused by the stretching of the ear drum. This pain is usually intense enough to stop the diver from descending further before a rupture of the eardrum occurs. Stopping the descent and ascending a few feet usually brings immediate relief. If the eardrum does rupture a sudden and violent onset of vertigo can occur causing disorientation and possibly nausea and vomiting. The vertigo is caused by the disturbance of the malleus, incus, and stapes or by cold water stimulating the balance mechanism of the inner ear. Fortunately these symptoms quickly pass and an ascent can be made. A middle ear squeeze can be prevented by not diving with partially blocked eustachian tubes. If you can't clear your ears on the surface don't dive. It is also a good idea to stay ahead of the pressure by descending slowly and making frequent adjustments of the middle ear pressure through the addition of air by means of the eustachian tubes. This is also important because the eustachian tube may collapse if the pressure differential is to great, making further attempts at pressure equalization impossible without first ascending to reduce the hydrostatic pressure. If, after a middle ear squeeze, symptoms such as continued pain, a feeling of fullness in the ear, hearing loss, or mild vertigo are noticed upon surfacing medical attention should be sought.
The sinuses are located within hollow spaces of the skull bones and are lined with mucous membranes. The location of the sinuses can be viewed by clicking here. These small air spaces are connected to the nasal cavity by narrow passages. If these passages are blocked by mucous or tissue growths, hydrostatic pressure will cause a sharp pain to be felt in the affected area. In an attempt to equalize this pressure imbalance the lining membranes will swell into the cavities and if severe enough hemorrhaging will occur. If no damage has occurred an ascent to a lesser depth will bring immediate relief and an attempt can be made to equalize the pressure by swallowing or blowing gently against the pinched off nose (Valsalva maneuver). If an equalization of pressure is not possible the dive must be aborted. In order to avoid a sinus squeeze dives should not be made while experiencing a cold or nasal congestion.
Tooth Squeeze (Barodontologia)
A tooth squeeze can occur when a small pocket of gas forms under a filling due to tooth decay. If no additional air can enter into this cavity the pulp of the tooth or the tissues in the tooth socket can be sucked into the space causing pain. A reverse squeeze can also occur if air enters the cavity on descent but cannot escape during ascent. This can cause the tooth to crack or the filling to be dislodged. Tooth squeezes can be prevented through regular dental check-ups and good dental work.
Air can be trapped in the ear canal if a diver wears ear plugs, a tight fitting wet suit hood, has an external ear infection or an ear canal which is blocked by ear wax. If this is the case, an external ear squeeze results when the ambient pressure exceeds the pressure of the gas trapped in the external ear canal. This causes the eardrum to bow outward in an attempt to equalize the pressure and at worst it can rupture. In addition, the skin of the ear canal swells and starts to hemorrhage causing considerable pain. An external ear squeeze can be prevented by not wearing ear plugs (which may also be pushed deeply into the ear canal) and ensuring that water can enter the wet suit hood. In addition divers should have their ears checked during their regular medical check ups.
Masks and some exposure suits can cause squeezes if they have enclosed spaces of air which cannot be equalized to match their pressure to the ambient pressure. Scuba masks can be equalized by breathing air into them through the nose. This is not possible with goggles. For this reason goggles should never be used for diving.
Middle Ear Overpressure (Reverse Middle Ear Squeeze)
During ascent expanding gas normally escapes through the eustachian tube. If the tube becomes blocked during ascent the air pressure in the middle ear will start to exceed the ambient pressure causing the eardrum to bow out. Apart from being painful this can cause the eardrum to rupture if the overpressure is significant. This causes the same symptoms as an eardrum rupture during descent. In rare cases this overpressure in the middle ear can also affect nearby structures causing vertigo and inner ear damage. If such symptoms occur during ascent or after surfacing it is extremely important to rule out an arterial gas embolism or decompression sickness. There is no guaranteed way to clear the ears on ascent. A Valsalva maneuver should not be attempted since this will only increase the pressure in the middle ear and worsen the symptoms. In general a diver should descend a short way to relieve the symptoms and then continue to ascend at a slower rate, gradually working his way to the surface. Diving with a cold increases the chances of developing this problem. This is also the reason why decongestants shouldn't be used while diving. If the decongestant stops working during the dive this problem is likely to occur.
Sinus Overpressure (Reverse Sinus Squeeze)
This occurs upon ascent if air is trapped in a sinus cavity and cannot escape. This can happen if a fold in the sinus membrane, a cyst, or a growth of the sinus membrane (polyp) acts as a check valve which traps the air inside. A sharp pain in the affected area is the result. This pain can be relieved by descending a few feet. The ascent should then continue slowly with the diver gradually working his way to the surface.
Overexpansion of the Stomach and Intestine
During a dive, gas may develop in the intestines or gas may be swallowed and become trapped in the stomach. On ascent this gas expands and may cause enough discomfort to force the diver to stop and expel gas. Continuing the ascent without doing this can cause damage to these organs.
A pressure imbalance between the middle ear and the surrounding environment can cause lasting damage to the inner ear mainly through a rupture of the round or oval window. This can occur if the imbalance is sudden or very large. The oval window is a membrane covered hole on the inner ear. This membrane is connected to the stirrup (stapes) one of three bones (hammer (malleus), anvil (incus), and stirrup (stapes)) in the middle ear (view graphic). These bones transmit and amplify the vibrations of the eardrum, caused by sound waves, to the inner ear by means of the oval window. Since the inner ear is filled with fluid there is a second membrane covered hole (the round window) whose elasticity is designed to relieve the pressure waves of the fluid moving in the inner ear due to these transmitted vibrations. Pressure imbalances can exert enough force on one of these membranes and the inner ear fluid to causes a tear in the other membrane. Through this tear, inner ear fluid then seeps into the middle ear. Such imbalances in the middle ear are caused mainly through very forceful Valsalva maneuvers. Symptoms of this injury are ringing or roaring in the affected ear, vertigo, disorientation, nystagmus, unsteadiness, and marked hearing loss.
These symptoms can sometimes be easily confused with arterial gas embolism or decompression sickness. Therefore the existence of an inner ear barotrauma should always be taken into consideration when these symptoms occur after dives in which a decompression sickness is unlikely. Recompression however cannot hurt and should be initiated if there is doubt regarding the cause of these symptoms. In all cases where inner ear barotrauma is suspected professional medical attention must be sought.
Pulmonary Overinflation Syndromes
Pulmonary overinflation syndromes are caused by pressure related injuries of the lungs. Such injuries can occur when:
there is excessive pressure in the lungs. This can occur when a diver takes a breath while pressing the purge button of his regulator.
The clinical manifestation of such an injury is dependent on the location of where the air escaping from the rupture in the alveolus collects (Click here to view a graphic chart of the possible consequences). In every case of a rupture, due to pulmonary overinflation, the air collects in the lung tissues first. This condition is known as interstitial emphysema but it causes no symptoms unless the air escapes further into the chest cavity or the arterial circulation.
This is potentially the most serious condition that can occur during diving. Arterial gas embolism can occur if expanding gas in the lungs causes a rupture of both the alveolar air sacs and surrounding blood vessels. This air is then forced into the pulmonary capillary bed. From here the air bubbles are carried to the left chamber of the heart where they can enter the arterial stream (see graphic). Bubbles that are too large to go through an artery form a plug (embolus) blocking this artery and stopping any further blood from flowing through. The tissues that this artery supplies are then deprived of the oxygen they need to continue functioning. The consequences of such a blockage depend on where the blockage occurs. If the brain is involved the condition is extremely serious being in essence a stroke which can cause lasting damages or death. Treatment calls for immediate recompression which reduces the size of the bubbles reinstating blood flow. To prevent this injury a diver must NEVER HOLD HIS BREATH WHILE DIVING and must make it a rule to breath normally and continually at all times! If breathing during ascent is not possible because of an out of air situation the diver must continuously exhale.
Mediastinal emphysema occurs when gas is forced through the torn lung tissues into the loose mediastinal tissues in the middle of the chest, around the heart, the trachea, and the major blood vessels (see graphic). This air can exert pressure on these organs, interfering with circulation and causing the victim to feel faint or short of breath.
Subcutaneous emphysema occurs when gas, which is forced into the mediastinal tissues, leaks into the subcutaneous tissues of the neck (see graphic). This air causes the victim to feel a fullness of the neck and to experience a change in voice. The skin of this area may also crackle when touched.
Pneumothorax occurs as a result of air entering the space between the lung and the wall of the chest. In its most common form (simple pneumothorax), a one time leakage of air from the lung into the chest partially collapses the lung, causing varying degrees of respiratory stress (see graphic). This condition normally improves with time as the leaked air is reabsorbed. In severe cases it may be necessary to remove the air from the chest cavity by means of a catheter. Symptoms of this condition include sharp chest pain, followed by difficult and rapid breathing, cessation of normal chest movements on the affected side, tachycardia (rapid heart beat), a weak pulse, and anxiety.
A rarer form of pneumothorax is known as tension pneumothorax. This occurs if the torn lung allows air to enter but not exit the chest cavity (see graphic). Continued breathing will steadily increase the pressure in the chest cavity, eventually causing a complete collapse of the affected lung as well as an impediment of circulation due to pressure on the heart. If not treated symptoms become progressively worse, beginning with rapid breathing and ending with cyanosis (bluish skin coloring due deficient oxygenation of the blood), hypotension (low blood pressure), shock, and, as the final result, death. All cases of pneumothorax require professional medical attention.
Under high partial pressures, inert gases cause anesthetic effects. This anesthesia impairs a diver's ability to think clearly. The most common form of inert gas narcosis is nitrogen narcosis which results from breathing compressed air at depth (typically starting at 30 meters/100 feet and becoming more pronounced at 45 meters/150 feet). Although the exact mechanisms which cause inert gas narcosis are not fully understood, theory suggests that nitrogen becomes dissolved in the lipids of nerve cells (neurons) and impedes the transmission of nerve signals. The symptoms of nitrogen narcosis include loss of judgment or skill, a false feeling of well-being, lack of concern for safety, apparent stupidity, euphoria, and tingling or numbness sensations of the lips, gums, and legs (see symptoms chart). Nitrogen narcosis is in and of itself not dangerous but the symptoms are. Especially the disregard for personal safety and the impaired judgment are very dangerous since they can result in a diver removing his regulator, descending to unsafe depths etc. The effects of narcosis recede rapidly upon ascension to shallower depths. In order to keep this hazard to a minimum, deep air dives should only be undertaken after proper training and acclimatization.
Oxygen at higher partial pressures than those encountered in the atmosphere can be toxic to the body. This toxicity is dependent on two factors: exposure time and degree of partial pressure. The are two different forms of oxygen toxicity:
1. Pulmonary Oxygen Toxicity: This low pressure oxygen toxicity can occur when a gas mix with more than 60% oxygen is breathed for longer than 24 hours. The symptoms begin with a burning sensation while breathing in and progress to pain during inhalation and coughing. Prolonged periods of exposure can lead to lung damage. This form of oxygen toxicity can be encountered during recompression treatments.
2. Central Nervous System (CNS) Oxygen toxicity: High pressure oxygen poisoning can occur when divers are exposed to oxygen partial pressures greater than 1.6 ata. With compressed air this can occur while diving at greater depths (> 66 meters with 21% oxygen in the air used for breathing). Since susceptibility varies from individual to individual and from dive to dive, an oxygen partial pressure of 1.4 ata is generally accepted as the safe upper limit. Symptoms include:
The most serious of these symptoms are convulsions. These can occur suddenly and without warning i.e. without the occurrence of any other symptoms. During a convulsion the individual loses consciousness and the brain sends out uncontrolled nerve impulses to the muscles. It goes without saying, that the consequences of this happening at depth on SCUBA can be severe.
Decompression sickness is due in part to the absorption of gases by the body under pressure. At sea level the average body contains about one liter of dissolved nitrogen. This is due to the fact that all body tissues are saturated with nitrogen at a partial pressure equal to that found in the alveoli, which is about 0.75 ata. If the partial pressure of nitrogen changes, for example because of breathing compressed air at depth, the pressure of the nitrogen dissolved in the body will gradually attain a matching level. As described in Henry's law the amount of gas that dissolves in a liquid is almost directly proportional to the partial pressure of that gas. If one liter of nitrogen is absorbed at a pressure of one atmosphere, then two liters are absorbed at two atmospheres and three liters at three atmospheres, etc. This process of taking up nitrogen is called saturation, the process of nitrogen elimination is called desaturation. The process for both is the same, except that the direction of the exchange is exactly opposite. In diving both processes occur, saturation due to the increased partial pressure of nitrogen at depth and desaturation during the return to the surface due to a decrease in the partial pressure of nitrogen. These same processes occur with helium and other inert gases used in a breathing mixture.
Decompression sickness occurs when the external pressure (for example through a rapid ascent) is decreased to a point where supersaturation of the tissues occurs. This is the case when the pressure of the gas dissolved in the tissues is higher than the total body pressure. When this happens the gas eventually separates from the solution forming bubbles. These bubbles can put pressure on the nerves, damage delicate tissues, and block the flow of blood to vital organs.
The symptoms of decompression sickness vary depending on where the bubbles end up in the body. Some of their direct effects can include:
The actual symptoms of DCS are dependant on the size and location of the bubbles. They include:
The treatment of decompression sickness requires recompression which reduces bubble size and alleviates symptoms if no lasting damage has occurred. The diver is then slowly decompressed to allow for a normal desaturation. This desaturation can be supported through a higher partial pressure of oxygen in the breathing air. The administration of oxygen is the recommended primary first aid for DCS.
Decompression sickness can be prevented by following the dive tables although a slight risk still remains since there are individual differences in susceptibility to DCS (for example due to age and amount of body fat). Susceptibility can also change from dive to dive due to the existence of predisposing factors such as dehydration, injuries, illnesses, alcohol consumption, water temperature and amount of exertion.
The following links lead to articles with further in depth information on diving physiology:
