HBOT for Carbon Monoxide Poisoning

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Of the three indicated and accepted conditions for routine treatment this one is the most confusing in how it’s treated. The condition must be acute before HBOT is indicated and commissioned for use in the UK. In other parts of the world health departments are less reluctant and it’s use is routine. It also important to note that not all CO poisoning is the kind that lands a person in A&E. Most of us live our daily lives with some level on contamination in the air we breathe. Even these moderate levels are akin to levels found in smokers. It has a direct effect on the oxygen carrying capability of the blood and can compromise metabolism.

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When carbon monoxide (CO) enters the lungs, it passes through the alveolar wall, consistent with normal gas exchange. Owing to a far greater affinity for CO by haemoglobin, it then displaces the oxygen attached to haemoglobin and attaches itself with greater voracity. Because this affinity is so high, oxygen under normal pressure (baric), cannot easily displace the CO and the blood carries less oxygen as a result. Even normal baric oxygen mask breathing is relatively unsuccessful in removing CO from haemoglobin or re-saturating it with oxygen.

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CO becomes the gate keeper and doesn’t allow oxygen saturation of red blood cells (RBC’s). Removal requires a higher inward pressure gradient than that exhibited by the CO, i.e. hyperbaric oxygenation. Oxygen must have a higher pressure compared to the CO binding to haemoglobin in order to displace it. This is similar to the way helium displaces nitrogen in trimix mixes because of higher affinity. CO displaces oxygen and requires increased pressure to reverse the carboxyhaemoglobin bond. Carboxyhaemoglobin is formed when CO bonds with haemoglobin. Oxygen must be at a higher pressure to become the favoured compound for haemoglobin bonding. (Hyperbaric oxygen therapy for carbon monoxide poisoning –Weaver 2014)


What’s more, a higher pressure of oxygen can also make use of the plasma as a means of transport as discussed, thus proving a bridging and potentially lifesaving therapy, in that it continues to supply vital systems and organs with oxygen despite haemoglobin being “bogged down”. When the haemoglobin has been successfully “scrubbed” of the CO, HBOT can cease as natural recovery will support itself.

It would eventually rectify naturally in mild cases, but takes a long time, all the while depriving the body of oxygen. Why deprive the body of oxygen? In cases where death is unlikely, it can still cause ill effects. Long term cognitive dysfunction among them. Why else would authorities insist on the compulsory placing of CO alarms almost everywhere in modern society. It’s that serious that even in mild cases it’s regarded as dangerous. The body simply doesn’t get the oxygen it has evolved to thrive with. This can continue for days or longer after a poisoning incident. Oxygen sensitive tissue can’t sustain that length of deprivation and still recover fully. Low oxygen should be regarded as serious as no oxygen. Duration of affliction becoming the deciding factor in determining the extent of cellular damage suffered. Shortening this window lowers the risk of any long term deficit.

The real danger with CO is that it is colorless, odourless and tasteless in and of itself. A victim could well have no idea that they are being poisoned and become unconscious suddenly, which, without help could very well lead to death. Cookers, fireplaces, heaters, vehicle exhaust emission and other gas or solid and liquid fuel combustion appliances are well known sources of carbon monoxide in the home. Usually however headache and maybe some nausea may be present. Also, a reddening of the nail beds. Similar could be said for carbon dioxide poisoning, although CO2 is easier to remove or scrub from the blood stream than CO. Ordinarily, unless life threatening, baric oxygen would alleviate and successfully treat carbon dioxide poisoning but not so for carbon monoxide.

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CO is so effective at depriving the brain and body of oxygen it quickly causes hypoxia, (hypoxia being the same resulting end condition suffered in low pressure altitude sickness), but rather more serious. Ultimately leading to death by asphyxia in the case of untreated serious carbon monoxide poisoning.
If we treat hypoxia in altitude sickness with increased pressure of oxygen, why not with all cases of CO poisoning, with maybe the exception of the mildest cases. The expected response for altitude sickness is to bring the victim to a place of higher pressure to resolve low oxygenation. Why does it have to be “Acute” with death being imminent before HBOT is commissioned for CO poisoning? The reason is that few hospitals have hyperbaric chambers or facilities, and often transporting a patient to a facility is ill advised, or such facility doesn’t meet the prescribed standard. Surely it is more cost effective to treat a victim of CO poisoning with HBOT over a shorter period than to have them as an in-patient for an extended period? In any available chamber?

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Yet It remains a condition not commissioned for the use of HBOT. One complication being the bureaucracy of requiring treatment in a type 1 or type 2 chamber, i.e. a hospital. Where self inflicted poisoning is suspected, even locked wards are preferred. A shame since there are a great many facilities which don’t have all this capability and hence are not allowed to administer HBOT to a victim of CO poisoning. It is agreed that a patient should receive hospital treatment, however provision should be made for ANY chamber to at least be able to offer immediate emergency treatment of victims followed then by proper hospitalisation. This early stage intervention can make the difference between retaining full brain function or not. Or indeed survival or death.

For this reason, among others, we plan to offer type 2 Care Quality Commission approved services.

Hayden Dunstan


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