Hyperlink to full size Cover Illustration.

SCUBA DIVING EXPLAINED

Questions and Answers on
Physiology and Medical Aspects of Scuba Diving

 

Lawrence Martin, M.D. Copyright 1997

 

Home
Buy the book
Scuba quiz
Myths & Misconceptions
Disclaimer & Invitation
FAQ's

Brief History of Diving
Recreational  Diving
The Respiratory System
Explanation of Pressure

Water & Physical Laws
Unequal Air Pressures
Decompression Sickness
Oxygen Therapy
Gas Pressure at Depth

Dive Tables & Computers
Stress & Diving
Non-air Gas Mixtures
Women & Diving
Medical Fitness for Diving
Asthma & Diving
The Great Debate

Glossary
All About DAN
Scuba Training Agencies
Magazines & Newsletters
Books & Videos

Diving Odds N' Ends

Internet Links




SECTION I

Effects of Gas Pressure at Depth: Nitrogen Narcosis, CO and CO2 Toxicity, Oxygen Toxicity, and "Shallow-Water Blackout"

WHAT HAPPENS TO GAS PRESSURES AT DEPTH?

Any gas taken to depth in a scuba tank will be unaffected as long as it remains in the tank. Once it leaves the tank and enters the diver's lungs it will have the same pressure as the surrounding water, i.e., the ambient pressure. This statement is true for the two major components of compressed air (nitrogen and oxygen), as well as for any gaseous impurities (e.g., carbon monoxide).

WHAT IS NITROGEN NARCOSIS?

Nitrogen narcosis, also called "rapture of the deep" and "the martini effect," results from a direct toxic effect of high nitrogen pressure on nerve conduction. It is an alcohol-like effect, a feeling often compared to drinking a martini on an empty stomach: slightly giddy, woozy, a little off balance.

Nitrogen narcosis is a highly variable sensation but always depth-related. Some divers experience no narcotic effect at depths up to 130 fsw, whereas others feel some effect at around 80 fsw. One thing is certain: once begun, the narcotic effect increases with increasing depth. Each additional 50 feet depth is said to feel like having another martini. The diver may feel and act totally drunk. Underwater, of course, this sensation can be deadly. Divers suffering nitrogen narcosis have been observed taking the regulator out of their mouth and handing it to a fish!

In The Silent World, Cousteau wrote about his early experiences with the aqua lung:

I am personally quite receptive to nitrogen rapture. I like it and fear it like doom.
It destroys the instinct of life. Tough individuals are not
overcome as soon as neurasthenic persons like me, but they have
difficulty extricating themselves. Intellectuals get drunk early and suffer
acute attacks on all the senses, which demand hard fighting to
overcome. When they have beaten the foe, they recover quickly. The
agreeable glow of depth rapture resembles the giggle-party jags of the
nineteen-twenties when flappers and sheiks convened to sniff nitrogen protoxide.

L'ivresse des grandes profoundeurs has one salient advantage over
alcohol no hangover. If one is able to escape from its zone, the brain
clears instantly and there are no horrors in the morning. I cannot read
accounts of a record dive without wanting to ask the champion how drunk he was.

The effect, thought due to a slowing of nerve impulses from inert gas under high pressure, is not unique to nitrogen; it can occur from many gases (though not helium). The effect is similar to what patients experience inhaling an anesthetic such as nitrous oxide (N2O). With increasing pressure of inhaled N2O there is a progression of symptoms, from an initial feeling of euphoria to drunkenness and finally to unconsciousness.

Every year there are diving deaths attributed to nitrogen narcosis, mainly among divers who exceed recreational depth limits. To prevent the problem commercial divers switch to a mixture of helium and oxygen (heliox) at depths exceeding around 170 fsw. Helium is much less soluble in tissues than nitrogen, and therefore is less likely to impair behavior (divers using helium still have to decompress to prevent DCS). Even setting aside the added cost and complexity, helium offers no advantage for recreational divers over ordinary air.

Because of similar (and additive) effects to excess nitrogen, alcohol should be avoided before any dive. A reasonable recommendation is total abstinence at least 24 hours before diving; by that time effects of alcohol should be gone.

Unlike the effects of alcohol, nitrogen narcosis dissipates quickly, as soon as the diver ascends to a safe level (usually less than 60 feet depth). There is also some evidence that some divers can become partially acclimated to the effects of excess nitrogen; the more frequently they dive the less each subsequent dive appears to affect them.

WHAT IS OXYGEN TOXICITY, AND CAN IT DEVELOP WHILE DIVING?

Oxygen toxicity is any injury or discomfort to the body from inhaling too much oxygen (see box). High concentrations of oxygen delivered at atmospheric pressure can harm the lungs. When diving, any given concentration of oxygen comes under higher pressure than atmospheric, thus increasing the amount inhaled and the potential for toxicity. Above atmospheric pressures, oxygen can also affect the central nervous system, and cause seizures and convulsions. Thus oxygen toxicity is a major potential hazard in some diving but not, as it turns out, recreational diving.

Oxygen is a vital gas, the absence of which leads to death in a few minutes. People with healthy lungs only need the amount of oxygen in the atmosphere, no more or less. Anything more than 21% oxygen is considered "supplemental oxygen."

Supplemental oxygen, like any drug, can be toxic at high doses; since oxygen is a gas the "dose" is based on both the percentage of oxygen inhaled and the ambient pressure. Patients who are ill from low blood oxygen receive a higher than normal percentage of oxygen as treatment (i.e., greater than 21%). Scuba divers, because of the increase in gas pressures with depth, inhale a higher than normal oxygen pressure; the percentage is the same, since compressed air is still 21% oxygen at any depth.

However, since pressure increases with depth, the deeper one dives the higher the total pressure of oxygen that is inhaled. Too high an inhaled oxygen pressure can be toxic to the lungs and central nervous system. Oxygen toxicity is the reason why very deep diving (e.g., greater than about 170 fsw) is safely accomplished not with compressed air, which contains 21% oxygen, but with a gas mixture that has a much lower percentage, e.g., 10% O2. Such a low oxygen percentage would be dangerous at sea level, but at great depth, due to the high ambient pressure, it is more than adequate to sustain life.

OXYGEN TOXICITY

Pulmonary effects (can occur at atmospheric pressure; threshold about 0.6 atm. O2)

  • burning sensation on taking a deep breath
  • cough
  • pneumonia
  • permanent lung damage

Central nervous system effects (requires pressures above atmospheric; threshold about 1.3 atm. O2)

  • muscular twitching
  • vomiting
  • dizziness
  • vision or hearing abnormalities
  • anxiety, confusion, irritability
  • seizures

Recreational scuba divers adhering to the dive tables have no significant risk of oxygen toxicity. At 35 feet depth, where RSD tables allow the diver to spend well over two hours on a non-repetitive dive, the PAO2 (oxygen pressure in the lungs) is the same as from breathing 43% oxygen at sea level, i.e., non-toxic. At the maximum RSD depth of 130 feet, the PAO2 from breathing compressed air is about the same as from breathing 100% oxygen at sea level. This level of oxygen would only begin to cause trouble if inhaled for at least an hour. The few minutes of bottom time that the tables allow at 130 fsw is simply not long enough to pose a significant risk from oxygen toxicity.

WHAT EXACTLY DETERMINES RISK OF OXYGEN TOXICITY?

The occurrence and type of oxygen toxicity correlate with the O2 concentration, the ambient pressure, the length of time supplemental O2 is inhaled, and the diver's level of activity.

Range of oxygen concentrations. The concentration of inspired oxygen can vary from zero to 100% (the maximum). The concentration in ordinary air is 21% (whether compressed or not, and regardless of the depth at which it is inhaled). The higher the concentration of O2 the greater the risk of oxygen toxicity.

Range of ambient pressures. Ambient pressure can range from zero (outer space), to one atmosphere (sea level), to several atmospheres (in a hyperbaric chamber or under water). On land, outside of a chamber, oxygen can be administered only at the surrounding atmospheric pressure, which can vary from 1 atmosphere (sea level) to about .33 atmosphere (summit of Mt. Everest). The higher the ambient pressure, the greater the risk of oxygen toxicity.

Length of time oxygen is inhaled. Supplemental oxygen can be given anywhere from a few seconds to lifelong. How long O2 is given depends on the condition being treated, the concentration used, and the ambient pressure. The longer supplemental oxygen is inhaled, the greater the risk of oxygen toxicity.

Level of activity. This is the least quantifiable aspect of oxygen toxicity. Once the threshold of oxygen toxicity is reached (based on atmospheres of O2), the more active the diver the greater the risk of developing actual toxicity.

Since air contains 21% oxygen, the amount of oxygen inhaled at sea level is .21 atm. O2; this amount is safe to breathe forever. From clinical experience it appears that patients can breathe .40 atm O2 indefinitely, and possibly up to .60 atm O2 for weeks at a time (equivalent to 40% O2 and 60% O2 at sea level, respectively), without apparent oxygen toxicity.

In healthy subjects, 100% oxygen at atmospheric pressure (1 atm. O2) causes chest discomfort, pain and cough after only a few hours. If inhaled continuously over 24 hours, 1 atm. O2 can lead to lung congestion (pulmonary edema) and, if continued, death. Obviously, doctors try not to use high concentrations of oxygen unless absolutely necessary. Patients who require 100% oxygen because of heart or lung disease are critically ill and will almost always be cared for in a hospital intensive care unit.

The most serious potential harm from inhaling supplemental oxygen at sea level pressure is lung injury, which develops slowly, over many hours. At depth the most serious harm from too much oxygen is a seizure, which can occur in just a few minutes of oxygen breathing.

HOW DO ATMOSPHERES OF O2 RELATE TO OXYGEN TOXICITY?

Although potentially toxic, 1 atm. O2 does not cause seizures. However, when 100% oxygen is delivered at pressures two or more times sea level pressure, the first toxic manifestation can be a seizure. A seizure is a sudden electrical discharge from the brain that causes uncontrolled muscle movement. If seizures occur under water the diver will likely be unable to breathe through the regulator and will drown (if rescue is not immediate).

Atmospheres of O2 is the major determinant of oxygen toxicity; the risk increases directly with the atmospheres of oxygen inhaled. A diver breathing compressed air (21% oxygen) at 4.76 atmospheres (124 fsw) has the same risk of developing oxygen toxicity as when breathing 100% O2 at sea level (assuming the same level of activity). In either situation the diver is breathing one atmosphere of oxygen (1 atm. O2).

Exposure to high oxygen pressures at RSD depths is not long enough to cause oxygen toxicity. Oxygen toxicity is mainly a concern for the deep diver, for divers breathing mixtures that contain more than 21% O2 (e.g., Nitrox), and for patients undergoing hyperbaric oxygen therapy. The thresh-old beyond which oxygen toxicity is a major concern is about 1.3-1.5 atm O2. The box shows some permutations for reaching this threshold.

1.3 atm O2 = 100% O2 at 9.1 fsw (pure oxygen)

32% O2 at 101 fsw (Nitrox)

21% O2 at 172 fsw (compressed air)

1.5 atm O2 = 100% O2 at 16.5 fsw (pure oxygen)

32% O2 at 122 fsw (Nitrox)

21% O2 at 203 fsw (compressed air)

 

1. When diving with compressed air, what is the percentage of inhaled oxygen at each of the following depths?
a. 33 fsw
b. 66 fsw
c. 99 fsw
2. When diving with compressed air, what is the atm. of inhaled oxygen at each of the following depths?
a. 33 fsw
b. 66 fsw
c. 99 fsw
3. A diver is treated at sea level, in an emergency room, with increasing concentrations of oxygen (provided via loose-fitting face masks). For each concentration of oxygen inhaled, state the amount in atm. O2.
a. 40%
b. 60%
c. 90%

TEST YOUR UNDERSTANDING Answers

HOW CAN OXYGEN TOXICITY BE MINIMIZED?

The risk of seizures from oxygen toxicity begins at 1.3 to 1.5 atm O2. To reach this level on compressed air the diver has to exceed the RSD depth limits (see box). Divers who go deep (technical or other) can reduce the risk of oxygen toxicity by decreasing the concentration of inhaled oxygen. For example, a diver at 7 atm. (198 fsw) might switch to a mixture containing just 4% oxygen (mixed with helium or helium and nitrogen). At sea level, 4% oxygen would not support human life; at 7 atm., 4% oxygen is about the same as breathing 28% oxygen at sea level. On the other hand, a diver breathing 21% oxygen at 7 atmospheres (198 fsw) would be at risk for oxygen toxicity as he would be inhaling 1.54 atm. O2.

Pure oxygen was used in re-breathing scuba equipment during World War II. Because of the risk of oxygen toxicity, military divers were limited to about 25 fsw, or 1.76 atm. O2. (The military now uses mixed gases with its re-breathing scuba apparatus for deeper diving). It is also because of oxygen toxicity that hyperbaric treatment schedules limit the breathing of 100% oxygen to only about 20 minutes at a time. In summary, the risk of oxygen toxicity is directly related to the total atm. of O2 activity. Examples of safe and unsafe oxygen concentrations are shown in Table 1.

TABLE 1. Risk of Oxygen Toxicity with Supplemental Oxygen*


Atm. O2 Inhaled
Time before O2 toxicity may develop** Depth equivalent in fsw breathing 100% O2 Depth equivalent in fsw breathing 21% O2 (compressed air)
0.21 never   0
0.42 indefinite   33
0.63 few hours   66
0.84 few hours   99
1.00 few hours sea level 124
1.30 mins to hours   9.1
  172 threshold***  
1.50 mins to hours   16.5
  203    
2.00 minutes 33 281
3.00 minutes 66 438
4.00 seconds 99 596
fsw = feet of sea water

* For the resting or sedentary individual; oxygen toxicity can develop more quickly with exercise

** Pulmonary or central nervous system effects

*** For risk of seizures

HOW DOES CARBON MONOXIDE TOXICITY OCCUR IN SCUBA DIVING?

Carbon monoxide (CO) is a tasteless, odorless, highly poisonous gas given off by incomplete combustion of petroleum fuel. Virtually every gasoline powered motor, including all cars that use hydrocarbon fuel, emit some carbon monoxide. All lighted cigarettes also give off carbon monoxide. The extreme toxicity of CO arises from the fact that, compared with oxygen, it combines about 200 times more readily with hemoglobin. As a result, any excess CO readily displaces some oxygen from the blood; the more CO there is, the more oxygen will be displaced.

CO-related problems while diving can occur two ways, one more infamous than the other. Probably the less appreciated problem is simply from smoking. All smokers (cigarette, cigar, pipe) have an elevated blood CO level and, sadly, many divers smoke (even on the dive boat!). There is no evidence that diving increases the blood CO level in smokers, but since CO competes with oxygen, the smoking diver is more hypoxic on entering and exiting the water than otherwise. Any stressful situation thus puts the diver at increased risk for an hypoxic-related event, such as heart attack.

While at depth, the hypoxic effect of excess CO will be somewhat (but not completely) mitigated by the higher blood oxygen level that also occurs at depth. In final analysis, we really don't know to what extent smoking causes problems in divers, but common sense (and basic physiology) makes it a dumb practice to smoke and dive.

The toxicity mechanism we hear more about is when enough CO is in the tank air to act as a life-threatening impurity. Fortunately this is a rare occurrence, but it happens, and the result can be truly disastrous. According to news reports in April 1994, soon after a German scuba diver's body was recovered off Key West, Florida,

"investigators suspected something unusual...analysis
[of air in the diver's tank] revealed
carbon monoxide nearly three times the level
considered acceptable."

The analysis reportedly showed 2500 parts per million of CO in the tank's air, an extraordinary level. Non-smoking city dwellers inhale about 10 p.m. (Ten p.m. is considered the maximal CO level permissible level in scuba tank air). Cigarette smokers inhale between 30 and 60 p.m. of CO; this amount binds from 5 to 10 per cent of the blood with CO, which means 5-10% of the smoker's blood is unable to carry oxygen. An inhaled CO level of 2500 would tie up over 60% of the blood and make anyone fatally hypoxic.

It was speculated that this diver's tank air was contaminated from a faulty air compressor. Air can certainly become impure when tank filling takes place near machine exhaust; the exhaust fumes can be taken up and compressed along with the surrounding air. At depth the pressure of any CO inhaled from a scuba tank is increased just like every other inhaled gas. However, unlike any other gas likely to be in the tank, even small amounts of CO can be harmful, because CO has a great affinity for hemoglobin and easily displaces oxygen from the blood.

Depending on the concentration of CO in the tank and the depth at which it is inhaled, the effects of CO toxicity may range from mild headache to confusion to a state of unconsciousness and death. Any CO impurity must be considered potentially dangerous at depth.

The incidence of faulty tank air is very rare, at least at reputable fill stations, so it is impractical to do on-site chemical analysis of every tank. Until air analysis becomes routine (if ever), testing must be up to the diver's senses, which means taking several breaths from the tank before entering the water. This practice helps provide a regulator check as well as a cursory check of the tank air. Certainly any headache (from CO) or bad taste (from other impurities) is warning that something may be wrong with the air. (Such a cursory check will likely not detect low levels of impurities, so sticking with a reputable fill station is probably your best protection.)

WHAT IS CARBON DIOXIDE TOXICITY?

Carbon dioxide is a gas byproduct of metabolism. Our body makes about 200 cc's of CO2 every minute (more when we exercise) and excretes it in the air we exhale. Plants take up the CO2 and give off oxygen (photosynthesis). The concentration of carbon dioxide in the atmosphere is almost zero, and poses no risk when fresh air is compressed inside a scuba tank.

The partial pressure of carbon dioxide in a scuba diver's blood is a function only of metabolism and the rate and depth of breathing the same factors that determine blood CO2 concentration on land. Unlike other gases normally inhaled (nitrogen and oxygen), or gases that could be inhaled under abnormal conditions (CO and other gas impurities), the CO2 level in the blood is unchanged by the ambient pressure (i.e., the depth) per se.

Scuba apparatus used in recreational diving is "open circuit," so exhalation of carbon dioxide is through the mouthpiece and into the water (it's all in the bubbles). Abnormal carbon dioxide accumulation in the blood can occur from too high a level of metabolism (from exercise) and/or inadequate breathing (usually not breathing deep enough). The medical term for high carbon dioxide in the blood is hypercapnia; when the level is high enough it can cause "CO2 toxicity," which can lead to shortness of breath, headache, confusion and drowning (depending on severity).

Air density increases with depth, so the deeper you go the greater the work of breathing. Increased resistance to breathing can cause the diver to take shallow breaths, and shallow breaths make carbon dioxide elimination less efficient. If the diver also exerts herself heavily, her body will produce more CO2, resulting in a "vicious cycle" of carbon dioxide buildup: heavy work (more CO2 production) ---> shallow breathing (less efficient elimination of CO2) ---> higher blood CO2 (CO2 toxicity).

Hypercapnia (and resulting CO2 toxicity) is a major concern among deep divers, and also any diver who has to perform heavy work. It is much less of a concern for the typical recreational diver. Regular, deep breathing, and a properly functioning regulator, should eliminate risk of carbon dioxide buildup in recreational diving.

Some experienced divers practice "skip" breathing, which is holding the breath (on inhalation or exhalation) in order to conserve air. This might save air but it could also lead to CO2 buildup, since by breath holding the diver is, in effect, under ventilating; if the diver under ventilates he will soon want to breathe even more, from the stimulus of an increasing CO2 level. As a result, the diver who skip breathes enough to increase his CO2 could end up depleting air supply faster than with normal breathing! Even without the obvious risk of pulmonary barotrauma (particularly if near the surface), skip breathing is definitely not recommended.

CO2 BUILDUP WHEN DIVING: RISKS

Diving deep
Heavy work
Rapid, shallow breathing
"Skip" breathing


Apart from the practice of skip breathing, for recreational divers the depths achieved, the short times spent on deeper dives, and the open circuit design of scuba equipment make CO2 toxicity an uncommon problem. Just be aware that, under some conditions, it can occur.

4. A diver breathing compressed air has a seizure after 10 minutes a 66 fsw. Until the onset of seizure he is observed to have no breathing difficulty or any problem with equipment. Rank the following potential causes of his problem from 1 (most likely cause) to 5 (least likely).
a. nitrogen narcosis
b. CO toxicity
c. CO2 toxicity
d. O2 toxicity
e. epilepsy (spontaneous seizures)
5. A diver breathing Nitrox I (32% oxygen, balance nitrogen) air has a seizure after 20 minutes at 140 fsw. Until the onset of seizure he is observed by his buddy to have no breathing difficulty or any equipment problem. Of the choices provided below, what is the most likely cause? Can the other four conditions be ranked as in the previous question?
a. nitrogen narcosis
b. CO toxicity
c. CO2 toxicity
d. O2 toxicity
e. Epilepsy
6. A diver breathing compressed air develops a headache after 20 minutes at 90 fsw. She is breathing fast and shallow and finds it difficult to inhale from her regulator. Tank psi is 1500 psi. The most likely cause of her headache is:
a. nitrogen narcosis
b. CO toxicity
c. CO2 toxicity
d. O2 toxicity
7. Of the choices a. through d. in question 6, which one is the least likely cause of the diver's headache?
8. A diver is at 130 fsw. hovering next to a wall, when he is seen to suddenly drift downward, seemingly oblivious to the increasing depth. His buddy catches up with him at 145 fsw and pulls him up to 100 fsw. The most likely explanation for the sinking diver's behavior is:
a. nitrogen narcosis
b. CO toxicity
c. CO2 toxicity
d. O2 toxicity

TEST YOUR UNDERSTANDING Answers

WHAT CAUSES HEADACHE UNDER WATER?

Many divers mistakenly believe that any headache under water is due to carbon dioxide buildup. For reasons discussed in the preceding section, CO2 buildup is uncommon in recreational divers. Even with CO2 buildup, head-ache may not be a symptom. In several studies the first symptom of CO2 buildup was sudden blackout, with no headache or other warning signs.

More importantly, there are many other (and more plausible) causes for a headache while diving. The potential causes include: tank gas impurities (e.g., low levels of carbon monoxide); temporomandibular (jaw) joint ache from holding the mouthpiece too tightly; pressure of the mask against the forehead; a tight mask strap; salt water in the nasal passages; tension or anxiety; cold water; over breathing (hyperventilation); and squeeze on inadequately ventilated frontal sinuses.

In summary, headache is a sign that something is not right, but (in recreational divers) it is not a sure sign of CO2 buildup.

WHAT IS SHALLOW-WATER BLACKOUT?

As has been pointed out, diving without compressed air (breath-hold diving, skin diving) is very different from scuba diving, since the lungs compress on descent and decompress on ascent. Water pressure squeezing the lungs during a breath-hold dive is usually not great enough to cause problems from compression of the lungs (most breath-hold divers don't go deep enough to experience significant lung squeeze). Middle ear discomfort is a more common problem, and the breath-hold diver must swallow or blow against a pinched nose to equalize ear pressures.

Since, in a breath-hold dive, air compressed on descent merely expands back to its original volume on ascent, there is no danger of pulmonary barotrauma. But breath hold diving is not without hazard. Perhaps the most serious potential hazard for the breath-hold diver is "shallow-water blackout."

Shallow-water blackout is a sudden unconsciousness from lack of oxygen during a breath-hold dive. (The term was originally applied, in the 1940s, to blackout from CO2 buildup seen with re-breathers; over the years the term's definition has been changed.) Shallow-water blackout doesn't always occur in shallow water; it can occur at any depth. However, for reasons which will be explained, the breath hold diver is at greater risk for blacking out during ascent, near the surface.

To appreciate shallow-water blackout, consider the air hunger you feel during a breath-hold dive. When you hold your breath two things happen in the blood; CO2 increases and O2 decreases. The principle reason you feel air hunger is the increase in CO2, not the decrease in O2. Without the slight increase in CO2 from breath holding, your sensation of air hunger would be delayed and you would stay down longer, even while your oxygen level is falling. This is an example where CO2 buildup is a good thing!

The risk of shallow-water blackout is increased from excessive over breathing (hyperventilation) just prior to the dive. Hyperventilation lowers blood CO2. At most one should take three to four deep breaths before a breath-hold dive; more than that can lower CO2 sufficient to delay its buildup and therefore the urge to breathe and surface for air. In other words, blood CO2 may be lowered so much by pre-dive hyperventilation, that it takes a relatively long time for CO2 to build up under water and cause "air hunger." The dive is prolonged but at the diver's peril. Blood oxygen will fall relatively quickly under water compared to the buildup of CO2. A critical hypoxic state can be reached before there is any drive to breathe, i.e., before there is any sensation of air hunger. This critical hypoxia is often reached on ascent, near the surface, hence the term "shallow-water blackout." However, it can occur at any depth and lead to sudden unconsciousness and drowning (Figure 1).

There is another factor that contributes to hypoxia, one that helps explain why blackout tends to occur near the surface. Even though the body utilizes oxygen throughout the breath hold dive, at depth the water pressure effectively increases oxygen pressure in the lungs and the blood. All the while, of course, the diver is metabolizing oxygen, so the total amount available is steadily declining. Paradoxically, however, being deep is somewhat protective, because the pressure of oxygen in the lungs and blood is higher than it would be at the surface with the same breath holding time. However, as the breath hold diver rises toward the surface, the pressure of oxygen in his lungs falls precipitously, not only because his body continues to utilize oxygen, but also because the surrounding pressure falls. Near the surface the breath-hold diver's blood oxygen pressure falls to a critical level and he blacks out. (Ambient pressure falls on ascent from a scuba dive as well, but the oxygen supply is continuously replenished with fresh air from the tank).

Figure 1. Example of changes in oxygen and carbon dioxide that can lead to shallow-water blackout in a breath-hold diver. Direction of arrows indicates PO2 and PCO2 values above (up) or below (down) normal land values. Initial changes show a diver who has hyperventilated just prior to the dive. Actual point at which PO2 and PCO2 reverse, and the degree of change, will depend on depth of dive, time under water, and work exerted on the dive.

A CASE OF "SHALLOW-WATER BLACKOUT"

A young scuba instructor working on a liveaboard dive boat, and one of the boat's male guests, decide to go breath-hold diving one afternoon. They, and two other boat guests along just for the ride, take a dingy out to the site of a famous wreck.

Each of the breath-hold divers carries four pounds of lead weight to assist in descent, and while one dives the other stays in the water as a spotter. While the non-diving guests remain in the dingy, the divers each make a breath hold plunge. The first dive for each lasts about 1.5 minutes, at a depth of 60 to 70 feet.

On the scuba instructor's second breath-hold dive, he goes a little deeper and stays on the wreck a little longer. Over 2 minutes into his dive, he is seen to ascend quickly from the wreck, then stop at 10 feet from the surface; at that point he shows no movement. The spotter dives down and drags the unconscious diver to the surface. The rescuing diver provides in-water mouth-to-mouth resuscitation and, with the aid of the two other people, lifts the by now semi-conscious diver into the dingy. The rescued diver fully regains consciousness but remembers nothing about what happened.

A few minutes later they are back on the liveaboard. The dingy observers reveal what an awful sensation they felt as the limp instructor was pulled to the surface; they thought he might be dead. The rescued scuba instructor only complains of having some chest discomfort and feeling fatigued. He is also observed to have blue nail beds (cyanosis). He is given 100% O2 and, when he claims to feel better, goes to lay down in his cabin. A few hours later he feels worse and has a fever; the captain decides to motor to the nearest town, where the diver is hospitalized. Diagnosis: pneumonia (presumably from aspiration of some sea water.) He is given antibiotics and the next day is released; he eventually recovers fully.

Youth, diving experience and excellent physical condition allowed the scuba instructor to stay down much longer than the average person; this was also his (almost fatal) undoing. What happened is that his delayed urge to breathe made him attempt an ascent too late; just 10 feet from the surface he blacked out from lack of oxygen. Had there not been an experienced spotter on the surface the instructor would surely have drowned.

Answers to TEST YOUR UNDERSTANDING

1. a, b, c. All are 21% Oxygen

2. a. .42 atm. O2
b. .63 atm, O2
c. .84 atm, O2

3. a. .40 atm, O2
b. .60 atm, O2
c. .90 atm. O2

4. 1st., epilepsy; 2nd., CO toxicity (due to contaminant in the tank air). These are the only two plausible causes among the five listed. CO2 toxicity would be unlikely due to the short time of the dive, the shallow depth, and the lack of a breathing or equipment problem. Nitrogen narcosis would also be unlikely at this depth. Oxygen toxicity would not occur at this depth after breathing compressed air for 10 minutes.

5. 1st. O2 toxicity. The other four causes are all possible but unlikely. Epilepsy can cause seizures at any time; a "first-ever" seizure under water is unlikely to be epilepsy, so the pre-dive medical history would be very important. CO2 toxicity usually does not present with seizures, but it can lower the threshold for developing oxygen toxicity. Nitrogen narcosis also does not acause seizures. Finally, CO toxicity is always a concern in sudeen and unexplained underwater castrophes, but it occurs only with major contamination of tank air.

6. c. Headache, fast and shallow breathing, and trouble inhaling from the reegulator all suggest CO2 toxicity.

7. d. O2 toxicity would be the least likely cause, since she has only spent 20 minutes at 90 fsw.

8. a. The diver went deep and lost concentration, a sure indication of nitrogen narcosis.

REFERENCES AND BIBLIOGRAPHY

See references Sections b-e, plus the following (*Especially recommended).

*Edmunds C, McKenzie B, Thomas R. Diving Medicine for Scuba Divers. J.L.
Publications, Melbourne, 1992.

*Gilliam B, Von Maier R. Deep Diving. An Advanced Guide to Physiology,
Procedures and Systems
. Watersport Publishing, Inc. San Diego; 1992.

Lanphier EH. Carbon dioxide poisoning, in Waite CL, ed., Case Histories of
Diving and Hyperbaric Accidents
, pages 199-213.

Lanphier EH, Rahn H. Alveolar gas exchange during breath hold diving.
J Appl Physiol 1963;18:471-477.

Lanphier EH, Rahn H. Alveolar gas exchange during breath holding with air.
J Appl Physiol 1963;18:478-482.

Lanphier EH. Breath-hold and ascent blackout. In The Physiology of Breath-hold Diving,
UHMS Pub. No. 72(WS/BH) 4/15/87, pages 32-43.

Leitch DR. A study of unusual incidents in a well-documented series of dives.
Aviation, Space, and Environ Med 1981;52:618-624.

*Lippmann J. Deeper into Diving Aqua Quest Publications, Inc., New York, 1992.

*Lippmann J. The Essentials of Deeper Sport Diving. Aqua Quest Publications,
Inc., New York, 1992.

Martin L. Hypercapnia Revisited. Sources, Journal of the National Association
of Underwater Instructors. November/December 1994, pages 52-54.

Pulmonary Medicine Home Page
e-mail: martin@lightstream.net
HTML Optimization by Richard F. Laporte

http://www.mtsinai.org/pulmonary/books/scuba/gaspress.htm
Last updated: 28/10/97