3-5 RESPIRATORY PROBLEMS IN DIVING

RESPIRATORY PROBLEMS IN DIVING

Physiological problems often occur when divers are exposed to the pressures of depth. However, some of the difficulties related to respiratory processes can occur at any time because of an inadequate supply of oxygen or inadequate removal of carbon dioxide from the tissue cells. Depth may modify these problems for the diver, but the basic difficulties remain the same. Fortunately, the diver has normal physiological reserves to adapt to environmental changes and is only marginally aware of small changes. The extra work of breathing reduces the diver’s ability to do heavy work at depth, but moderate work can be done with adequate equipment at the maximum depths currently achieved in diving.

Oxygen Deficiency (Hypoxia).

Oxygen deficiency, or hypoxia, is an abnormal deficiency of oxygen in the arterial blood that causes the tissue cells to be unable to receive sufficient oxygen to maintain normal function. Severe hypoxia will stop the normal function of any tissue cell in the body and will eventually kill it, but the cells of the brain tissue are by far the most susceptible to its effects.

The partial pressure of oxygen determines whether the amount of oxygen in a breathing medium is adequate. For example, air contains about 21 percent oxygen and thus provides an oxygen partial pressure of about 0.21 ata at the surface. This is ample, but a drop to 0.14 ata causes the onset of hypoxic symptoms on the surface. If the ppO2 goes as low as 0.11 ata at the surface, most individuals become hypoxic to the point of being nearly helpless. Consciousness is usually lost at about 0.10 ata and at much below this level, permanent brain damage and death will probably occur. In diving, a lower percentage will suffice as long as the total pressure is sufficient to maintain an adequate ppO2. For example, 5 percent oxygen would render a ppO2 of 0.20 ata for a diver at 100 fsw. On ascent, however, the diver would rapidly experience hypoxia if the oxygen percentage were not increased.

Causes of Hypoxia.

The causes of hypoxia vary, but all interfere with the normal oxygen supply to the body. For divers, interference of oxygen delivery can be caused by:

• Equipment problems such as low partial pressure of oxygen in the breathing mix, inadequate gas flow, inadequate purging of breathing bags in a closed oxygen UBA like the LAR V, or blockage of the fresh gas injection orifice in a semiclosed-circuit UBA.

• Blockage of all or part of the pulmonary system air passages by vomitus, secretions, water, foreign objects, or pneumomediastinum.

• Pneumothorax or paralysis of the respiratory muscles from spinal cord injury.

• Decreased oxygen exchange at the alveoli/capillary membrane caused by accumulation of fluid in the tissues (edema), a mismatch of blood flow and alveolar ventilation, lung damage from near-drowning or smoke inhalation, or “chokes” or bronchospasm from lung irritation due to showers of bubbles in the circulation.

• Physiological problems such as anemia and inadequate blood flow that interfere with blood transportation of oxygen. Edema can interfere with gas exchange at the capillary/tissue areas, and carbon monoxide poisoning can interfere with oxygen utilization at the cellular level.

• Hyperventilation followed by breathholding, which can lead to severe hypoxia. Hyperventilation lowers the carbon dioxide level in the body below normal (a condition known as hypocapnia) and may prevent the control mechanism that stimulates breathing from responding until oxygen tension has fallen below the level necessary to maintain consciousness. Extended breathholding after hyperventilation is not a safe procedure. Refer to paragraph 3-7 for more information on hyperventilation and its hazards.

Symptoms of Hypoxia.

Brain tissue is by far the most susceptible to the effects of hypoxia. Unconsciousness and death can occur from brain hypoxia before the effects on other tissues become very prominent.

There is no reliable warning of the onset of hypoxia. It can occur unexpectedly, making it a particularly serious hazard. A diver who loses his air supply is in danger of hypoxia, but he immediately knows he is in danger and usually has time to do something about it. He is much more fortunate than a diver who gradually uses up the oxygen in a closed-circuit rebreathing rig and has no warning of impending unconsciousness.

When hypoxia develops, pulse rate and blood pressure increase as the body tries to offset the hypoxia by circulating more blood. A small increase in breathing may also occur. A general blueness (cyanosis) of the lips, nail beds and skin may occur with hypoxia. This may not be noticed by the diver and often is not a reliable indicator of hypoxia, even for the trained observer at the surface. The same signs could be caused by prolonged exposure to cold water.

If hypoxia develops gradually, symptoms of interference with brain function will appear. None of these symptoms, however, are sufficient warning and very few people are able to recognize the mental effects of hypoxia in time to take corrective action.

Symptoms of hypoxia include:

• Lack of concentration
• Lack of muscle control
• Inability to perform delicate or skill-requiring tasks
• Drowsiness
• Weakness
• Agitation
• Euphoria
• Loss of consciousness

Treating Hypoxia.

A diver suffering from severe hypoxia must be rescued promptly. Hypoxia’s interference with brain functions produces not only unconsciousness but also failure of the breathing control centers. If a victim of hypoxia is given gas with adequate oxygen content before his breathing stops, he usually regains consciousness shortly and recovers completely. For scuba divers, this usually involves bringing the diver to the surface. For surface-supplied mixed-gas divers, it involves shifting the gas supply to alternative banks and ventilating the helmet or chamber with the new gas. Details of treatment are covered in volume 3.

Preventing Hypoxia.

Because of its insidious nature and potentially fatal outcome, preventing hypoxia is essential. In open-circuit scuba and helmets, hypoxia is unlikely unless the supply gas has too low an oxygen content. On mixed-gas operations, strict attention must be paid to gas analysis, cylinder lineups and predive checkout procedures. In closed- and semiclosed-circuit Underwater Breathing Apparatus (UBA), a malfunction can cause hypoxia even though the proper gases are being used. Electronically controlled, fully closedcircuit UBA like the MK 16 have oxygen sensors to read out oxygen partial pressure, but divers must be constantly alert to the possibility of hypoxia from UBA malfunction. Oxygen sensors should be monitored closely throughout the dive in closed-circuit mixed gas MK 16 UBA. MK 25 UBA breathing bags should be purged in accordance with Operating Procedures (OPs). Recently surfaced mixed-gas chambers should not be entered until after they are thoroughly ventilated with air.

Carbon Dioxide Toxicity (Hypercapnia).

Carbon dioxide toxicity, or hypercapnia, is an abnormally high level of carbon dioxide in the body tissues.

Causes of Hypercapnia.

In diving operations, hypercapnia is generally the result of a buildup of carbon dioxide in the breathing supply or in the body caused by:

• Inadequate ventilation of surface-supplied helmets

• Excess carbon dioxide in helmet supply gas (failure of CO2 absorbent canister) in mixed-gas diving

• Failure of carbon dioxide absorbent canisters in closed- or semiclosed-circuit UBA

• Inadequate lung ventilation in relation to exercise level (caused by controlled breathing, excessive apparatus breathing resistance, increased oxygen partial pressure, or increased gas density)

• Any cause of increased dead space, such as shallow and rapid breathing through a snorkel

  Symptoms of Hypercapnia.

  Underwater breathing equipment is designed to keep the carbon dioxide below 1.5 percent during heavy work. The most common cause of hypercapnia is failure to ventilate helmets adequately. This can occur through improper breathing techniques or excessive breathing resistance; a diver can poison himself by inadequately ventilating his lungs. This happens primarily when a scuba diver tries to conserve his breathing supply by reducing his breathing rate below a safe level (skip-breathing). Inadequate lung ventilation is more common in diving than in surface activities for two reasons. First, some divers have a lower drive to increase lung ventilation in the face of increased blood carbon dioxide levels. Second, the usually high ppO2 encountered in diving takes away some of the uncomfortable shortness of breath that accompanies inadequate lung ventilation.

  Hypercapnia affects the brain differently than hypoxia does. However, it can result in similar symptoms such as confusion, inability to concentrate, drowsiness, loss of consciousness, and convulsions. Such effects become more severe as the degree of excess increases. A diver breathing a gas with as much as 10 percent carbon dioxide generally loses consciousness after a few minutes. Breathing 15 percent carbon dioxide for any length of time causes muscular spasms and rigidity.

  A diver who loses consciousness because of excess carbon dioxide in his breathing medium and does not aspirate water generally revives rapidly when given fresh air. He usually feels normal within 15 minutes and the aftereffects rarely include symptoms more serious than headache, nausea, and dizziness. Permanent brain damage and death are much less likely than in the case of hypoxia.

  Effects of Increasing Carbon Dioxide Levels.

  The increasing level of carbon dioxide in the blood stimulates the respiratory center to increase the breathing rate and volume, and the heartbeat rate is often increased. Ordinarily, increased breathing is definite and uncomfortable enough to warn a diver before the ppCO2 becomes very dangerous. However, variables such as work rate, depth, and the composition of the breathing mixture may produce changes in breathing and blood mixture that could mask any changes caused by excess carbon dioxide.

  This is especially true in closed-circuit UBA (especially 100-percent oxygen rebreathers) when failure or expenditure of the carbon dioxide absorbent material allows a carbon dioxide buildup while the amount of oxygen increases. In cases where the ppO2 is above 0.5 ata, the shortness of breath usually associated with excess carbon dioxide may not be excessive and may go unnoticed by the diver, especially if he is breathing hard because of exertion. In these cases the diver may become confused and even slightly euphoric before losing consciousness. For this reason, a diver must be particularly alert for any marked change in his breathing comfort or cycle (such as shortness of breath or hyperventilation) as a warning of hypercapnia.

  Effects of Excess Carbon Dioxide.

  Excess carbon dioxide also dilates the arteries of the brain. This may partially explain the headaches often associated with carbon dioxide intoxication, though these headaches are more likely to occur following the exposure than during it. The increase in blood flow through the brain, which results from dilation of the arteries, is thought to explain why carbon dioxide excess speeds the onset of oxygen toxicity or possibly convulsions. Excess carbon dioxide during a dive is also believed to increase the likelihood of decompression sickness, but the reasons are less clear. Headache, cyanosis, unusual sweating, fatigue, and a general feeling of discomfort may warn a diver if they occur and are recognized, but they are not very reliable as warnings.

  Hypothermia also can mask the buildup of carbon dioxide because the respiration rate increases initially on exposure to cold water. Additionally, nitrogen narcosis can mask the condition because a diver under the effects of narcosis would not notice any difference in his breathing rate. During surface-supplied air dives deeper than 100 fsw (30.5 meters), the Diving Supervisor must ensure the divers maintain sufficient ventilation rates.

  Treating Hypercapnia.

  Hypercapnia is treated by relieving the excess partial pressure of carbon dioxide. This is accomplished in surface-supplied diving by ventilating the helmet with fresh air in an air diving apparatus, bypassing the carbon dioxide absorbent in a mixed-gas diving apparatus, or ascending. Any method used to decrease the partial pressure removes the problems encountered with excess carbon dioxide.

  Asphyxia.

  Asphyxia indicates the existence of both hypoxia and carbon dioxide excess in the body. Asphyxia occurs when breathing stops. Breathing stoppage can be due to injury to the windpipe (trachea), the lodging of an inhaled object, the tongue falling back in the throat during unconsciousness, or the inhalation of water, saliva, or vomitus.

  In many situations, hypoxia and carbon dioxide excess occur separately. True asphyxia occurs when hypoxia is severe or prolonged enough to stop a diver’s breathing and carbon dioxide toxicity develops rapidly. At this point the diver can no longer breathe.

  Breathing Resistance and Dyspnea.

  The ability to perform useful work underwater depends on the diver’s ability to move enough gas in and out of his lungs to provide sufficient oxygen to the muscles and to eliminate metabolically produced carbon dioxide. Increased gas density and breathing apparatus resistance are the two main factors that impede this ability. Even in a dry hyperbaric chamber without a breathing apparatus, the increased gas density may cause divers to experience shortness of breath (dyspnea). Dyspnea usually becomes apparent at very heavy workloads at depths below 120 fsw when a diver is breathing air. If a diver is breathing helium-oxygen, dyspnea usually becomes a problem at heavy workloads in the 850-1,000 fsw range. At great depths (1,600-1,800 fsw), dyspnea may occur even at rest.

  Causes of Breathing Resistance.

  Flow resistance and static lung load are the two main causes of the breathing limitations imposed by the underwater breathing apparatus. Flow resistance is due to a flow of dense gas through tubes, hoses, and orifices in the diving equipment. As gas density increases, a larger driving pressure must be applied to keep gas flowing at the same rate. The diver has to exert higher negative pressures to inhale and higher positive pressures to exhale. As ventilation increases with increasing levels of exercise, the necessary driving pressures increase. Because the respiratory muscles can only exert so much effort to inhale and exhale, a point is reached when further increases can not occur. At this point, metabolically produced carbon dioxide is not adequately eliminated and increases in the blood, causing symptoms of hypercapnia.

  Static lung load is the result of breathing gas being supplied at a different pressure than the hydrostatic pressure surrounding the lungs. For example, when swimming horizontally with a single-hose regulator, the regulator diaphragm is lower than the mouth and the regulator supplies gas at a slight positive pressure once the demand valve has opened. If the diver flips onto his back, the regulator diaphragm is shallower than his mouth and the regulator supplies gas at a slightly negative pressure. Inhalation is harder but exhalation is easier because the exhaust ports are above the mouth and at a slightly lower pressure.

  Static lung loading is more apparent in semiclosed- and closed-circuit underwater breathing apparatus such as the MK 25 and MK 16. When swimming horizontally, the diaphragm on the diver’s back is shallower than the lungs and the diver feels a negative pressure at the mouth. Exhalation is easier than inhalation. If the diver flips onto his back, the diaphragm is below the lungs and the diver feels a positive pressure at the mouth. Inhalation becomes easier than exhalation. At high work rates, excessively high or low static lung loads may cause dyspnea without any increase in blood carbon dioxide level.

  Preventing Dyspnea.

  The U.S. Navy makes every effort to ensure that UBA meet adequate breathing standards to minimize flow resistance and static lung loading problems. However, all UBA have their limitations and divers must have sufficient experience to recognize those limitations. If the UBA does not impede ventilation, the diver’s own pulmonary system may limit his ability to ventilate. Whether due to limitations of the equipment or limitations imposed by the diver’s own respiratory system, the end result may be symptoms of hypercapnia or dyspnea without increased carbon dioxide blood levels. This is commonly referred to as “overbreathing the rig.”

  Most divers decrease their level of exertion when they begin to experience dyspnea, but in some cases, depending on the depth and type of UBA, the dyspnea may continue to increase for a period of time after stopping exercise. When this occurs, the inexperienced diver may panic and begin to hyperventilate (breathe faster than is necessary for the exchange of respiratory gases), which increases the dyspnea. The situation rapidly develops into one of severe dyspnea and uncontrollable hyperventilation. In this situation, if even a small amount of water is inhaled, it can cause a spasm of the muscles in the larynx (voice box) called a laryngospasm, followed by asphyxia and possible drowning. The proper reaction to the dyspnea is to stop exercising, ventilate the UBA if possible, take even, controlled breaths until the dyspnea subsides, evaluate the situation and then proceed carefully. Generally, soreness of the respiratory muscles is the only prominent aftereffect of a dive in which breathing resistance is high.

  Carbon Monoxide Poisoning.

  Carbon monoxide in a diver’s air supply is dangerous. Carbon monoxide displaces oxygen from hemoglobin and interferes with cellular metabolism, rendering the cells hypoxic. Carbon monoxide is not found in any significant quantity in fresh air; carbon monoxide pollution of a breathing supply is usually caused by the exhaust of an internal combustion engine being too close to a compressor intake. Concentrations as low as 0.002 ata can prove fatal. Carbon monoxide poisoning is particularly treacherous because conspicuous symptoms may be delayed until the diver begins to ascend.

  While at depth, the greater partial pressure of oxygen in the breathing supply forces more oxygen into solution in the blood plasma. Some of this additional oxygen reaches the cells and helps to offset the hypoxia. In addition, the increased partial pressure of oxygen forcibly displaces some carbon monoxide from the hemoglobin. During ascent, however, as the partial pressure of oxygen diminishes, the full effect of carbon monoxide poisoning is felt.

  Symptoms of Carbon Monoxide Poisoning.

  The symptoms of carbon monoxide poisoning are almost identical to those of other types of hypoxia. The greatest danger is that unconsciousness can occur without reliable warning signs. When carbon monoxide concentration is high enough to cause rapid onset of poisoning, the victim may not be aware of weakness, dizziness, or confusion before he becomes unconscious. When toxicity develops gradually, tightness across the forehead, headache and pounding at the temples, or nausea and vomiting may be warning symptoms.

  Treating Carbon Monoxide Poisoning.

  The immediate treatment of carbon monoxide poisoning consists of getting the diver to fresh air and seeking medical attention. Oxygen, if available, should be administered immediately and while transporting the patient to a hyperbaric or medical treatment facility. Hyperbaric oxygen therapy is the definitive treatment of choice and transportation for recompression should not be delayed except to stabilize the serious patient prior to transport. The air supply of a diver suspected of suffering carbon monoxide poisoning must be secured to prevent anyone else from breathing it and the air must be analyzed.

  Preventing Carbon Monoxide Poisoning.

  Carbon monoxide poisoning can be prevented by locating compressor intakes away from engine exhausts and maintaining air compressors in the best possible mechanical condition.