Decompression sickness could be avoided by breathing just pure oxygen. And the usage of higher concentrations of oxygen in breathing mixtures not only facilitates metabolic function, but also aids in the washout of inert gases such as nitrogen and helium. Despite the beneficial effects of breathing oxygen at higher concentrations, oxygen proves to be toxic in excessive amounts, and over cumulative time intervals. Too little oxygen is equally detrimental to the diver. As practiced, limits to oxygen partial pressures in breathing mixtures range, 0.16 atm to 1.6 atm, roughly, but symptoms of hypoxia and hyperoxia are dose dependent. Or, in other words, symptom occurrences depend on oxygen partial pressures and exposure times, just like inert gas decompression sickness. The mixed gas diver needs to pay attention not only to helium and nitrogen in staged decompression, but also cumulative oxygen exposure over the dive, and possible underexposure on oxygen depleted breathing mixtures. The neurotoxic actions of high-pressure oxygen are thought to relate directly to biochemical oxidation of enzymes, either those linked to membrane permeability or metabolic pathways. The list below is not exhaustive, but includes the following mechanisms:

1. The inability of blood to remove carbon dioxide from tissue when hemoglobin is oxygen saturated.
2. Inhibition of enzymes and coenzymes by lipid peroxides.
3. Increased concentration of chemical free radicals, which attack cells.
4. Oxidation of membranes and structural deterioration reducing electrical permeability for neuron activation.
5. Direct oxygen attack on smooth muscle fibres.
6. Oxygen induced vasoconstriction in arterioles.
7. Elevation of brain temperature due to lack of replacement of oxygen by carbon dioxide in hemoglobin.
8. And, simple chemical kinetic redistribution of cellular carbon dioxide and oxygen with high surrounding oxygen tensions
Fortunately for the diver, there are ways to avoid complications of hyperoxia. Careful attention to dose (depth-time) limitations for oxygen exposures is needed. Despite the multiplicity and complexity of the above, limits for safe oxygen exposure are reasonably denied.
Table 1 below lists NOAA CNS oxygen exposure time limits, tχ , for corresponding oxygen partial pressures, pO2. Below 0.5atm, oxygen toxicity (CNS or pulmonary) is not really a problem.
Figure 1 depicts these oxygen partial pressure limits for pulmonary and neurological toxicity manifestations, suggested by the US Navy and Lambertsen. Recent working NOAA limits

The CNS data in Table 1 is easily fitted to a dose time curve, using least squares, yielding, or, equivalently, in the same units, that is pO2 and tχ in atm and min respectively. The last column tabulates a pulmonary exposure dose, Υ, for divers, called the oxygen tolerance unit (OTU), developed by Lambertsen and coworkers at the University of Pennsylvania. Formally, the oxygen tolerance, Υ, is given by, and can be cumulatively applied to diving exposures according to the following prescriptions


1. Maintain single dive OTUs below 1440min on the liberal side, or allow for 690 min of that as possible full DCI recompression treatment on the conservative side, that is, 750 min.

2. Maintain repetitive total dive OTUs below 300min.

The expression is applied to each and all segments of a dive, and summed accordingly for total OTUs, and then benchmarked against the 750 min or 300 min rough rule. The 750 min and 300 min OTU rules are not cast in stone in the diving community, and 10% to 25% variations are common, in both conservative and liberal directions. Formally, if Υn is the oxygen tolerance for the nth the segment of a dive, with segment time, tn , and oxygen partial pressure, pnO2, the total OTU accumulated, Υ, is

with N the total number of dive segments (multilevel, deco, repetitive). Originally, Lambertsen defined a unit pulmonary toxicity dose (UPTD), Φ, given by,

weighing oxygen partial pressure more than the OTU, but the definitions share the same basis, though slightly different fits to oxygen dose data. In the diving community, both representations have their proponents, favoring the oxygen partial pres- sure or time in oxygen dose estimations. For exceptional and multiple exposures, the USN and University of Pennslyvania suggest the limits summarized in Table 2, where for multiple exposures, N, and segment times, tx

Note the severe reduction in multiple oxygen exposure time at 1.6 atm in Table 2. For this reason, technical divers generally restrict mixed gas diving exposures to PO 2 < 1:6 atm through- out any sequence of dives.

There are many ways to measure oxygen, with devices called oxygen analyzers. They are em- ployed in chemical plants and refineries, hyper- baric chambers, intensive care units, and nurseries. The paramagnetic analyzer is very accurate, and relies on oxygen molecular response to a magnetic field in displacing inert gases from collection chambers. Thermal conductivity analyzers differentiate oxygen and nitrogen conduction properties in tracking temperatures in thermistors, with difference in temperatures proportional to the oxygen concentration.

Magnetic wind analyzers combine properties of paramagnetic and thermal analyzers. Polarographic analyzers measure oxygen concentration by resistance changes across permeable oxygen membranes. Galvanic cell analyzers are microfuel cells, consuming oxygen on touch and generating a small current proportional to the amount of oxygen consumed. In all cases, analyzer response is linear in oxygen concentration. Although it is tempting to avoid problems of oxygen toxicity by maintaining oxygen partial pressures, pO2 , far below toxic limits, this is not beneficial to inert gas elimination (free or dissolved state). Higher levels of inspired oxygen, thus correspondingly lower levels of inert gases, are advantageous in minimizing inert gas buildup and maximizing inert gas washout. Coupled to narcotic potency of helium and nitrogen, and molecular diffusion rates, balancing and optimizing breathing mixtures with decompression requirements is truly a complex and careful technical diving exercise.

For the diver, all the foregoing translates into straightforward oxygen management protocols for both CNS and pulmonary toxicity. They are similar to inert gas management, but individual susceptibilities to oxygen seem to vary more widely, though reported statistics are more scattered.

Consider CNS oxygen management first, using the CNS clock as it is popularly termed, and then pulmonary oxgen management, using the OTU as described.

  1. CNS Toxicity Management

The various oxygen time limits, tχ, tabulated in the Tables, obviously bound exposures, t, at oxygen partial pressure, PO 2 . Converting the exposure time to a fraction of the limit, Ξn, we can define a CNS oxygen clock, Ξ, that is over N exposure levels,


for exposure time, tχ, at level, n, with oxygen time limit, tχn. Tabulating Ξ is most easily done by a computer. The prescription might be, depending on degree of conservatism,

and where Ξ = 1 is the nominal choice. The fit equation for PO 2 and tχ suffices to range estimates of Ξ across all depths.

For repetitive dives, a surface interval penalty, similar to the nitrogen penalty in the USN Tables, can be levied for oxygen. A 90 min halftime is employed today, that is, the decay constant for residual oxygen CNS management, λO 2 , is

For surface interval, t, initial CNS clock, Ξ, and for 90 min folding time, the penalty (or residual) CNS clock, Ξ, is simply,

The residual value is added to the planned repetitive dive additively, just like nitrogen penalty bottom time.

2. Pulmonary Toxicity Management

Pulmonary oxygen toxicity, Υ,follows a similar management scheme. As described, the total exposure, Υ, is the sum of interval exposures, Υn,

and is limited, 300 min Υ 750 min depending on the desired degree of conservatism, and multiplicity of repetitive dives. Variation of 15% to 25%
in the exposure limits are common.