Oxygen is the most basic life support system our bodies employ, and yet also has the capacity to cause great harm. Keller (1946) has called oxygen “The Princess of Gases. She is beautiful but has to be handled with special care”. We cannot live without it, but in prolonged breathing exposures or in deep depths on standard air scuba systems too much of a good thing can prove fatal.
Thom and Clark (1990) note, “paradoxically, the same gas that is required to sustain life by preventing loss of consciousness and death from hypoxemia has toxic properties that affect all living cells at sufficiently high pressure and duration of exposure.” Most divers are familiar with the basic characteristics of oxygen as it occurs in our atmosphere. It is a colorless, odorless and tasteless gas found free in dry air at 23.15% by weight and 20.98% by volume. For discussion purposes, we will consider its volume percentage to be 21%. Interestingly, the relative toxic effects of oxygen are determined not by the percentage in any mixed gas (including standard air at approximately 21% oxygen and 79% nitrogen), but by the oxygen partial pressure (PO2).
A review of Dalton’s Law of Partial Pressures is helpful (The total pressure exerted by a gas mixture is equal to the sum of the partial pressures of the components of the mixture i.e. P = P1+P2+P3…etc.), but put simply, as depth increases a corresponding elevation in the partial pressure of oxygen is achieved and must be considered by any diver planning deeper exposures. At the surface we are naturally adapted to PO2 at .21 atmospheres absolute (ATA). This is considered the reference point for “normoxic” conditions.
It is important to be aware of certain ranges of tolerance in normal, healthy persons. Most people can maintain proper blood oxygenation down to .16 ATA (16% oxygen in the mix at surface pressure) but dropping much below this will limit performance/endurance and unconsciousness will likely result approaching .1 ATA (10% oxygen at the surface).
As a physics reminder please note that we commonly refer to the percentage of a gas in any mixture as the Fg (fraction of the gas expressed as the decimal equivalent); thusly the FO2 at the surface can be correctly expressed as .21; Pg or partial pressure of a gas may be expressed as the Fg multiplied by atmospheres absolute or ATA’s. Therefore, the PO2 at 66 fsw is properly expressed as .63 ATA of O2. This is derived from multiplying .21 (the FO2 of oxygen in AIR) by the pressure in ATA’s: .21 X 3 = .63 ATA’s of O2. Though the FO2 will remain constant, the PO2 will increase with depth.
The diver may recall the old reference to the “Ten and Ten Rule” wherein it supposed that blackout will occur if the percentage of either oxygen or carbon dioxide (C02) reaches 10% in the gas mixture. This was particularly important to competitive free divers and spearfisherman while holding their breath and attaining depths in excess of 80 to 100 fsw (24.2 to 30.3 m). Many of these individuals could reach far deeper depths through applied disciplines of hyperventilation and adaptation in conjunction with techniques employed to precipitate the “diving reflex” to extend time underwater. This practice, however, is a double edged sword: as depth increased carbon dioxide was produced by the body’s metabolism, and absent any other source of oxygen, this “O2 storage” advantage was depleted. To a certain degree this was counterbalanced by a corresponding rise in the percentage of CO2 in the system since this gas is a metabolic waste product as O2 is burned.
The relationship is important because high CO2 is a major stimulus to breathe while low O2 is not. As the diver held his breath, O2 was consumed and CO2 eventually said, “Hey buddy, I’ll continue to hurt you unless you get back to the surface and get a fresh breath, you idiot!” Now the insidious danger occurs. As the diver ascended, both partial pressures dropped accordingly. His stimulus to breathe was reduced as PCO2 dropped while his PO2 could be dropping to dangerous levels.
At some point, the diver passed out from this “latent hypoxia” syndrome or what became commonly known as “shallow water black out”. Typically the diver showed no signs or distress and simply went limp, sometimes within ten feet of the surface. Those who were successfully rescued and revived related no warning of the impending blackout or any major stimulus to breathe. But several fatalities were sustained before the problems were identified and the hazards of deep breath-hold diving were well communicated.
CENTRAL NERVOUS SYSTEM O2 TOXICITY (Paul Bert Effect)
For the free swimming scuba diver, the most immediate dangers with O2 toxicity are encountered in deeper depths where the PO2 exceeds 1.6 ATA (218 fsw); in military, commercial and some scientific applications the ideal method of controlling the toxic effects of O2 are to keep the oxygen dose as near “normoxic” as possible. This is accomplished by controlling the gas mixtures. A typical mix would reduce the oxygen percentage in a deep dive usage and let the elevated pressure raise the PO2 to normoxic levels. For example,if a diver needed a mix for the 300 fsw (91 m) level the O2 could be used at only 2% with another inert gas. The affect of 10 ATA’s at 300 fsw would produce a PO2 of .21 ATA, the same as we normally breathe at the surface. The dive supervisor could select a single inert gas such as helium (He) or combine two inert gases such as nitrogen and helium while keeping the O2 percentage constant. The resulting gas mixes are commonly referred to as HELIOX or TRIMIX respectively. Realistically however, this mix would incur a greater decompression obligation due to the elevated inert gas percentages if oxygen was kept at an FO2 of .20; a .10 to .15 FO2 would be more practical.
Since traditional activities are for divers using standard air as the breathing gas, we shall consider that we do not have the luxury of custom mixing our oxygen percentages. Our gas is going to be 21% O2 and 79% nitrogen and we are stuck with it unless the diver makes the commitment to mixed gas equipment and its attendant responsibilities. As AIR divers we will be most concerned with the acute phase of oxygen toxicity (sometimes also referred to as oxygen poisoning). Acute O2 toxicity for well experienced and “depth adapted” divers will ultimately be the deciding factor in penetration limits, not inert gas narcosis.
The central nervous system is primarily affected in the acute phase and the following table will illustrate typical manifestations.
SIGNS AND SYMPTOMS OF CNS O2 TOXICITY IN NORMAL MEN
- Facial pallor
- Sweating
- Bradycardia
- Palpitations
- Depression
- Apprehension
- Visual symptoms:
- Dazzle
- Constriction of visual field
- Tinnitus and auditory hallucinations
- Vertigo
- Respiratory changes
- Nausea
- Spasmodic vomiting
- Fibrillation of lips
- Twitching of: lips, cheeks, nose, eyelids
- Syncope
- Convulsions
CNS O2 TOXICITY SYMPTOMS (VENTID)
Vision: any disturbance including “tunnel vision,” etc.
Ears: any changes in normal hearing function
Nausea: severity may vary and be intermittent
Twitching: classically manifest in facial muscles
Irritability: personality shifts, anxiety, confusion etc.
Dizziness: vertigo, disorientation
Even a cursory examination of these effects should illustrate the seriousness of a CNS O2 hit in deep water. Onset and severity of symptoms do not follow any particular pattern and may vary in an individual diver from day to day. Of particular note is that there may be no warning with less serious symptoms before full convulsion is precipitated. Thom and Clark (1990) observe that “minor symptoms did not always precede the onset of convulsions, and even when a preconvulsive aura did occur, it was often followed so quickly by seizures that it had little practical value”.
Many divers have relied on the incorrect supposition that lip twitching or “eye ticks” would provide adequate notice of impending disaster but this has been disproved by chamber tests and direct observation in actual dive scenarios. It is strongly suspected that CNS O2 toxicity and/or severe narcosis played the major role in the loss of almost a dozen divers in the last two decades while attempting record dives on standard air.
Oxygen convulsions, per se, are not inherently harmful but imagine the implications for an untended diver or even one with a buddy near by. Management of a patent airway and rescue in such an extreme situation is near impossible and the diver will almost certainly drown.
Mount (1991) related a near miss accident he was inadvertently involved in during a deep dive in 1971. He was diving at the 330 fsw (100 m) level and in control of narcosis with no O2 toxicity problems when he observed an obviously out of control female diver blissfully pass him with a vigorous kick cycle heading straight down! He gave chase and intercepted her near the 400 fsw (121.2 m) level. Making contact and arresting her plunge required heavy exertion and power kicking strokes to initiate ascent for the pair. “Within seconds after this effort, I had almost complete visual collapse. I found myself looking through a solid red field with black spots; basically blind. I made it up to the 300 fsw (90.9 m ) level with her and was relieved in the rescue by other divers. By 275 fsw (83.3) I was getting occasional ‘windows’ but my vision did not return to normal until past 250 fsw (75.8).”
I also witnessed another case while diving on a scientific project in the Virgin Islands in 1972. My regular buddy and I were gathering samples at 290 fsw (87.9) as part of an on-going survey. We were both well adapted from daily deep diving and routinely worked this depth without difficulty. On this occasion, another scientist diver had joined us at his request. In prior discussions, he had satisfied us that he was familiar and experienced with deep diving procedures. About seven minutes into the dive we watched him begin hammering away on a coral sample for retrieval and suddenly go limp. I caught him as he started to fall over the drop-off wall and ventilated him with his regulator’s purge valve while rapidly ascending. At 190 fsw (57.6 m) he completely recovered and began breathing on his own. He was unable to recall anything except beginning work with his hammer. This incident finally stopped the university’s practice of forcing outsiders on our professional teams. It was sheer luck that I happened to be looking his way when he passed out.
Most cases of underwater blackout result in death. The dangers of this type of CNS O2 toxicity cannot be too greatly emphasized. On AIR, at 300 fsw (91 m) or 10 ATA, the PO2 has reached 2.1 ATA; this partial pressure will definitely produce toxicity limited only by time and other influences such as elevated PCO2.
For these indisputable facts, the practice of AIR diving deeper than 300 fsw (91 m) must be placed in the perspective of assumable risk of sudden death not just injury.
It should be noted that divers routinely push nearly 3 ATA pf O2 in recompression chambers for extended periods. Theoretically, chamber divers are supposed to be at rest but many of the bounce dive profiles practiced by extreme deep AIR divers include performance plans that essentially have the diver “at rest” in the water with negative descents and controlled buoyant ascents in the toxicity range.
Neither Watson and Gruener (1968) or the author (1990) suffered O2 toxicity problems on their record dives to 437 and 452 fsw (132.4 and137 m) respectively but their times in the critical toxicity zone were limited and they each had practiced exceptional adaptive techniques. (In spite of this, Watson and Gruener reported near total incapacitation due to narcosis.)
When I was involved in very deep diving on projects in the late 1980s that ended up leading to setting a new record for depth in February 1990 at 452 feet, I believed that adaptation was proven to narcosis as well as to onset of O2 toxicity and was able to effectively limit narcosis impairment. But my primary concern from the very beginning was O2 toxicity. My tables were based on fast descents and fast ascents in the “Tox zone.” I felt I could tolerate up to five minutes below 300 feet and still get out before the high PO2 would hit me. In retrospect, of course, it worked.
Other factors in my success include almost absurdly low respiration and heartbeat rates, repeated progressive deep exposures and limited physical exertion. Like narcosis, O2 toxicity can be precipitated by higher CO2 levels generated in work tasks or simply swimming harder. Deep divers need to develop strong disciplines for energy conservation and focused breathing habits. The double whammy of sudden onset and increased severity of narcosis and CNS O2 toxicity in a stress situation can rapidly accelerate a borderline control situation into a disaster. The U.S. Navy still conducts oxygen tolerance tests in dry chambers to screen individuals with unusual susceptibility to O2. However, highly motivated individuals may escape detection anyway. Both Mount and Rutkowski have served as chamber supervisors and conducted such tests. In 1991 when interviewed, neither could recall any instances where a pre-screening O2 tolerance test was failed. The validity of such test protocols remains debated.
The following table gives the oxygen partial pressure limits during working dives as recommended by NOAA. This will provide some parameters for dive planning and is deliberately conservative. The scuba diver should be safe within these limits presuming good physical fitness and no predisposition to toxicity such as heavy smoking habits or asthma conditions. No guarantee of safety can ever be presumed.
NOAA PO2 And Exposure Time Limits for Working Divers
Normal Exposure Limits
_____________________________________________
Feet of Seawater Oxygen Partial Max. Duration Max.Total
fsw Pressure (PO2) For Single Duration,24
in ATA Exposure,in min. hr.day,in min.
218 1.6 45 150
203 1.5 120 180
187 1.4 150 180
171 1.3 180 210
156 1.2 210 240
140 1.1 240 270
124 1.0 300 300
108 .9 360 360
93 .8 450 450
77 .7 570 570
61 .6 720 720
Exceptional Exposures
______________________________________________________
281 2.0 30
266 1.9 45
250 1.8 60
234 1.7 75
218 1.6 120
203 1.5 150
187 1.4 180
171 1.3 240
Given the now mainstream usage of nitrox mixtures and other mixed gases that may provide oxygen in the mixture at a greater or lessened percentage than that of air at an FO2 of .21, the following table has been provided as a handy reference for maximum depths on various FO2 to remain within recommended limits of exposure.
MAXIMUM DEPTHS FOR A GIVEN FO2 GIVEN A LIMITING PO2
__________________________________________________
FO2 1.4 ATA 1.6 ATA
fsw fsw
0.15 275.00 319.00
0.16 255.75 297.00
0.17 238.76 277.59
0.18 223.67 260.33
0.19 210.16 244.89
0.20 198.00 231.00
0.21 (normoxic) 187.00 218.43
0.22 177.00 207.00
0.23 167.87 196.57
0.24 159.50 187.00
0.25 151.80 178.20
0.26 144.69 170.08
0.27 138.11 162.56
0.28 132.00 155.57
0.29 126.31 149.07
0.30 121.00 143.00
0.31 116.03 137.32
0.32 111.37 132.00
0.33 107.00 127.00
0.34 102.88 122.29
0.35 99.00 117.86
0.36 95.33 113.67
0.37 91.86 109.70
0.38 88.58 105.05
0.39 85.46 102.38
0.40 82.50 99.00
0.41 79.68 95.78
0.42 77.00 92.71
0.43 74.44 89.79
0.44 72.00 87.00
0.45 69.67 84.33
0.46 67.43 81.78
0.47 65.30 79.34
0.48 63.25 77.00
0.49 61.29 74.76
0.50 59.40 72.60
As in the case of Table 5-3 these depths are recommendations based on normal working conditions for the diver. In the case of gases mixed for purposes of decompression, it may possible for some divers to use deeper depths on higher FO2 values. Consult experts before attempting such higher exposures.
CHRONIC OXYGEN TOXICITY ( Lorraine Smith Effect )
This effect was commonly referred to in the past as pulmonary toxicity. Rutkowski makes frequent reference in his lectures to the diver’s “pulmonary clock.” In the early 1990s, the term “whole body” toxicity also came into use.
This phase of O2 toxicity is less a problem for divers except in prolonged in-water oxygen decompression or in actual recompression therapy. This “chronic” toxicity is generally associated with longer, low pressure exposures as compared to the high PO2 values encountered at depth. Due to the limits of extended hyperbaric oxygen breathing, a method of calculating the individual total O2 exposure incurred during all phases of a dive was developed. This can also be used to factor decompression and O2 treatment breathing periods. This measure is known as the Unit Pulmonary Toxicity Dose (UPTD) and tables are available for calculating UPTD’s for AIR, pure O2 and mixed gases.
Hamilton (1989) notes in his REPEX paper, “The Pennsylvania unit (UPTD) has served well and is based on empirical data; it is the basic unit used in the Repex method. For two reasons, however, we prefer to use an alternative term: OTU or Oxygen Tolerance Dose. First, since we are dealing with operational physiology in managing exposure to oxygen in diving we prefer to refer to these as techniques for ‘tolerance’ of O2 exposure, rather than for avoiding O2 ‘toxicity’. They are the same thing, but we feel it offers a more positive approach.”
The OTU and its predecessors are calculated by the following expression:
OTU = t [(PO2 – 0.5) / 0.5] 0.83
where t is the duration of the exposure in minutes and PO2 is the oxygen partial pressure in ATA. The 0.5 ATA is the “threshold” below which no significant symptoms develop; even oxygen injured lungs can recover below this level. (Bardin and Lambertsen 1970 and Eckenhoff et al. 1987) The exponent 0.83 was determined to give the best fit to the data on reduction of vital capacity as a function of oxygen exposure. An important benefit of this method is that the units are additive, and the net result of multiple short exposures can be totalled.
These dose tolerances were calculated originally for divers in multi-day saturation missions; scuba divers are urged to consult with experts in O2 management before attempting any dives where significant OTU doses will be accumulated. Because of the nature of the REPEX operation its algorithm does not devote much attention to acute CNS toxicity specifically. It is intended that divers just stay out of the CNS toxicity zone by staying below 1.5 ATA PO2. As a general rule of thumb, the daily OTU dose should always be calculated to allow the diver to sustain a full treatment Table 6 (approximately 650 OTU/UPTD) if necessary. Refer to the NOAA Table for suggested exposures at specific depths/ATA PO2 for scuba divers. By referencing between these two tables, the accumulated OTU dose can be accurately tracked.
For isolated or single day exposures, an 850 OTU dose can be tolerated. Second day exposures drop to a recommended 700 OTU dose level and continue to fall off over multi-day exposures. The reader is referred to Hamilton’s original REPEX work for additional information.
Chart of OTU dose by PO2 and air depths. The values in the Table from left are the PO2, depth in fsw or msw diving with air to give that PO2,and the number of OTU per minute at the indicated PO2 level. To calculate a dose, multiply the value in the chart for the exposure PO2 by the number of minutes of the exposure. For exposures at different PO2’s, calculate the dose in OTU for each exposure at a given PO2 and sum the OTU’s to get the total exposure.
|
PO2 atm or bar |
DEPTH fsw |
DEPTH msw |
OTU/ min |
|
0.50 |
45.6 |
13.8 |
0.00 |
|
0.55 |
53.4 |
16.2 |
0.15 |
|
0.60 |
61.3 |
18.6 |
0.27 |
|
0.65 |
69.1 |
21.0 |
0.37 |
|
0.70 |
77.0 |
23.3 |
0.47 |
|
0.75 |
84.9 |
25.7 |
0.56 |
|
0.80 |
92.7 |
28.1 |
0.65 |
|
0.85 |
100.6 |
30.5 |
0.74 |
|
0.90 |
108.4 |
32.9 |
0.83 |
|
0.95 |
116.3 |
35.2 |
0.92 |
|
1.00 |
124.4 |
37.6 |
1.00 |
|
1.05 |
132.0 |
40.0 |
1.08 |
|
1.10 |
139.9 |
42.4 |
1.16 |
|
1.15 |
147.7 |
44.8 |
1.24 |
|
1.20 |
155.6 |
47.1 |
1.32 |
|
1.25 |
163.4 |
49.5 |
1.40 |
|
1.30 |
171.3 |
51.9 |
1.48 |
|
1.35 |
179.1 |
54.3 |
1.55 |
|
1.40 |
187.0 |
56.7 |
1.63 |
|
1.45 |
194.9 |
59.1 |
1.70 |
|
1.50 |
202.7 |
61.4 |
1.78 |
|
1.55 |
210.6 |
63.8 |
1.85 |
|
1.60 |
218.4 |
66.2 |
1.92 |
|
1.65 |
226.3 |
68.6 |
2.00 |
|
1.70 |
234.1 |
71.0 |
2.07 |
|
1.75 |
242.0 |
73.3 |
2.14 |
|
1.80 |
249.9 |
75.7 |
2.21 |
|
1.85 |
257.7 |
78.1 |
2.28 |
|
1.90 |
265.6 |
80.5 |
2.35 |
|
1.95 |
273.4 |
82.8 |
2.42 |
|
2.00
|
281.3 |
85.2 |
2.49
|
Symptoms of chronic pulmonary O2 toxicity include shortness of breath, fatigue, dry coughing, lung irritation and a burning sensation in the breathing cycle. Pulmonary edema is most common and a marked reduction in vital capacity.
In treatments in recompression chambers, patient tenders also look for irritability in the patient or unreasonable disposition as early warning signs that dictate an AIR break in the schedule to allow some relief period. Bennet (1991) expressed concern over sport divers’ use of in-water O2 decompression as possibly becoming a post-dive factor if treatment should be required later. This relates to the so-called “oxygen box” where a patient reaches the UPTD limit and can no longer tolerate O2 therapy and leaves the chamber supervisor in a quandry for a viable exit protocol. This reflected an incomplete practical knowledge of exposures and his opinion was largely rebutted by field professionals.
From a practical standpoint, pulmonary or “whole body” effects are virtually impossible to sufficiently accumulate using open circuit equipment so that they become a factor in diving planning. Some instructors with an incomplete understanding of tracking the OTU dose have mistakenly concluded that precise measurement of such units is necessary. Hamilton emphasizes that this REPEX tracking theory was designed for divers in saturation with no opportunity to return to the surface and normal oxygen pressures during the multi-day period. Thus the importance of multi-day dose accumulations became crucial to planning. However, open circuit divers eventually will have to return to the surface, if only to sleep and eat. That period is adequate to allow sufficient “blow off” time to re-set the pulmonary clock to, essentially, zero each day. In almost any foreseeable dive plan, the CNS limits will always be the controlling oxygen clock. You can prove this yourself by simply adding the OTUs for any given dive and you’ll find that just to obtain 300 OTUs or more would require a superhuman dive profile that violates the exposure recommendations for the CNS clock so grossly as to make the pulmonary considerations moot.
However, it must be emphasized that accurate tracking of the CNS clock is crucial. This includes both the bottom depth exposure and the decompression phase. Several accidents have occurred because divers planned only for the “depth” phase of the dive and forgot the consequences of breathing oxygen or high O2 percentage nitrox during decompression.
Here’s an example:
A dive to 220 fsw on air for 30 minutes is allowable while staying inside the 45 minute single dive exposure for oxygen at 1.6 ATA. However, 88 minutes of decompression will be required (using U.S. Navy tables). Assuming the deeper stops were taken on air, it would be a common mistake for some divers to think they could safely switch to pure oxygen for the 20 foot stop. The table calls for 23 minutes at this depth. But wait: oxygen at 20 fsw brings the diver right back to 1.6 ATA again and this would place him 8 minutes over the maximum recommended limit. Convulsive events have been precipitated for precisely these types of failures to calculate the total dosage. What’s the solution? Drop the decompression phase PO2 by utilizing an 80/20 nitrox mix which will keep the exposure at or below 1.4 ATA.
So what’s happening with the pulmonary “whole body” clock? Not much. The bottom phase of the dive on air loaded about 60 OTUs and even if the entire decompression phase was taken on varying mixtures to yield a uniform 1.4 ATA O2 exposure, only about 140 OTUs would be added there. This totals right about 200 OTUs for what is a decidedly aggressive dive by any criteria. Remembering that you can take up to 850 OTUs per day (and still provide an allowance of 650 OTUs should you need to reserve them for a DCS treatment). 200 OTUs doesn’t really amount to anything. In fact, you could do this same profile four more times before you ran out of exposure time on the pulmonary clock. However, the reality is that you would blow the CNS limits off the gauge and probably bend yourself as well.
So if you’ve been staying up nights worrying about calculating OTUs, relax. They’ll take care of themselves just fine if you stay within the CNS guidelines.
SUMMARY
Both manifestations of oxygen toxicity can play a role in the deep diver’s plan. Of most concern is the extremely dangerous and unpredictable CNS O2 Tox hit at depth. Divers should exercise extreme caution when venturing beyond the 1.6 ATA range and penetrations beyond 275 fsw (83.3 m) on AIR are ill-advised except in the most experienced and adapted diver.
Unlike narcosis impairment, where a quantifiable possibility of rescue exists from an alert buddy or self-recognition of problem levels can be relieved by ascent, an O2 hit can quickly progress to uncontrollable convulsive states and drowning. As divers become more attuned to management of inert gas narcosis, the O2 toxicity barrier will be the ultimate depth limit.
I cannot emphasize enough that a thorough understanding of the technical physiology issues and a comfort level in calculating the exposure is vital to any diving activity. Most current diving training programs make no effort to go into detail on this subject or to explain it adequately. Seek out a proper curriculum such as that through Technical Diving International (TDI) or simply avoid the thresholds of deeper depths entirely.
Caution is the guiding rule. Avoid Darwin’s Rule at all costs…
Another detailed and excellent article! I feel like reading a wikipedia page of Oxygen in Diving gas mixtures. Very informative.