Last week, a worrying report made the rounds on diving forums: an Italian tech diver discovered helium contaminated with carbon monoxide (CO) in the diluent before a CCR dive in Sharm el Sheik. Do we now always have to analyze our gas for CO?
It is suspected that it was contaminated gas imported from Russia, where the quality standards are low. However, this is speculation. What is clear, though, is that the concentration of 88 ppm (parts per million, 0.0088% vol.%) could have had potentially catastrophic consequences.
The concentration of CO in a gas or the environment is given in ppm (parts per million). "Clean" air contains 0.1 ppm CO. The normal value in a home is 0.5 to 5 ppm (e.g. wood fire; 5 ppm = 0.0005 vol.%). The maximum permissible workplace concentration is 30 ppm (max. 42 h/week). The Euro standard EN12021 specifies that breathing gas must not contain more than 5 ppm CO.
CO is invisible, odourless and is oxidized to CO2 in the atmosphere. CO can contaminate breathing gas in the the following ways (non-exhaustive list):
Aspiration of exhaust gases from incomplete combustion of hydrocarbons
Oil pyrolysis: CO is produced in the final stage at temperatures > 200°C from oil in contaminated compressors
"Cracking": complex hydrocarbon molecules from oil residues in diving bottles are broken down into smaller molecules via chemical processes under heat and/or pressure
Smoke from cigarettes and cigars
Low-quality distillation of helium during extraction from natural gas
The production of nitrox by gas separation using a permeable membrane, for example, further increases the number of CO molecules in the gas. The production of 40 percent Nitrox increases the CO concentration by up to 3 times.
CO has the following effects in the organism:
CO drives oxygen away from haemoglobin (Hb), its transport protein in the erythrocytes (red blood cells), by occupying it with an affinity 240 times stronger than O2. This reduces the blood's O2 transport capacity.
CO changes Hb in such a way that it is less capable of releasing O2 in the tissues.
CO impairs O2 utilization by blocking key proteins in cellular respiration. This effect is particularly strong in the heart, whose function is impaired as a result.
CO produces harmful waste products from O2 that can directly damage proteins and cells, especially neurons.
CO poisoning leads to internal suffocation due to obstruction of O2 transport, O2 release to the tissues and O2 utilization in the vital organs (e.g. heart).
It also leads to long-term sequelae due to damage to the nervous system caused by reactive O2 species.
The extent of CO poisoning depends on the concentration of CO and oxygen in the breathing gas, the duration of exposure and the ventilation rate (the respiratory minute volume, AMV). The higher these are, the greater the percentage of Hb that is occupied by CO (%CO-Hb). This percentage correlates roughly with the severity of the symptoms (table 1).
ppm | %CO-Hb | Effects on organism |
<5 | 1 | None |
10 | 1.8 | None |
30 | 5 | None |
60-150 | 10-20 | Headache, breathlessness |
150-300 | 20-30 | Vertigo, nausea, impaired dexterity |
300-650 | 30-50 | Nausea, confusion, loss of consciousness |
650-1000 | 50-65 | Coma, fatal if untreated |
>1000 | >65 | Fatal |
Table 1: AMV 20 l/’, 1 h exposition
DAN recommends a maximum of 5 ppm CO in the breathing gas. Why not 10 ppm, which is still safe? Because this value means that there is probably a source of CO in the area of the compressor that needs to be searched for. Or because the origin of the supplied gas must be checked.
CO-poisoned persons do not turn blue, but remain rosy.
The diagnosis must be made on site, e.g. in the case of fires, based on the circumstances. It is important to know that CO poisoned patients do not "turn blue" as is usually the case with O2 deficiency, but remain pink. In the emergency ward, the %CO-Hb can be determined relatively easily in the blood. If there is the slightest suspicion, high doses of O2 must be administered at the scene of the accident. In cases of severe CO poisoning, the treatment of choice is hyperbaric oxygen therapy ("hyperbaric chamber treatment"), which displaces CO from Hb. In this way, the half-life of CO-Hb decreases from 4-6 h under air breathing to approx. 1.5 h at 1 bar O2 and to 30 minutes at approx. 2.5 bar O2.
Emergency therapy: high-dose oxygen or pressure chamber treatment
The problem with diving is that Dalton's law also applies to CO. This means that as the ambient pressure increases, the pressure of CO also increases proportionally.
For example, if the breathing gas is contaminated with a CO concentration of 30 ppm and is dived to 30 m (4 bar ambient pressure), the amount of CO that reaches the Hb also increases 4-fold. This would correspond to a CO concentration of 120 ppm at the water surface with a resulting CO-Hb of 17%, which leads to symptoms.
Due to Dalton's law, the effect of the CO concentration is multiplied during the dive.
The good news is that this is counteracted by the increased partial pressure of oxygen during diving. The increased dissolved O2 can support the supply of oxygen to the tissue, while CO-Hb transports less O2. This is why divers can remain asymptomatic at depth.
During the ascent, however, the oxygen partial pressure and thus the amount of dissolved O2 decreases. However, this does not apply to CO-Hb, as it is a chemical bond. It can be assumed that divers who have breathed CO at depth are therefore at the highest risk of losing consciousness on ascent, as they then lose the protection provided by the increased partial pressure of O2 at depth. However, the toxic limits of CO at depth and their modification by different ambient and O2 partial pressures have not been established.
When breathing CO, the risk of unconsciousness is greatest due to the drop in O2 partial pressure at the end of the dive.
Smoking 1 pack of cigarettes a day leads to a CO-Hb of approx. 3 -6 %. This "baseline" value must be added in the case of CO poisoning. Smokers are therefore at a disadvantage in the event of CO poisoning compared to non-smokers.
If we take the 88 ppm CO mentioned at the beginning and assume that a tech dive had been carried out at 60 m, this would correspond to an equivalent of approx. 600 ppm CO at the surface (7 x 88 ppm). Even if we assume that the high O2 setpoint of the rebreather (approx. 1.2 bar PO2) would counteract this, it is easy to see that the dive could have ended in disaster.
Do we now also have to consistently measure the CO in the breathing gas and if so, how? Even expensive gas analyzers for tech diving do not offer a function for CO. However, separate CO analyzers are available for a few hundred swiss francs.
The use of a CO analyzer is recommended for diving world travelers.
If you buy gas from reputable suppliers in our part of the world, you hardly need to worry about excessive CO pollution. The situation is different if you dive across the rest of the world. This apparently starts in diving hotspots in Egypt. As the example shows, it is worth analyzing the breathing gas yourself, especially if you do not know the source of the breathing gas or how it is processed. This applies to all breathing gases, including CO. The investment in the CO analyzer was undoubtedly worthwhile for the affected diver.
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