Carbon monoxide blood levels

Lethal concentrations (LC50S) for inhalation of carbon monoxide blood agents have not been fully established. However, immediately dangerous to life or health levels (IDLHs) for inhalation of these agents are as low as 2 ppm. 

A casualty with known exposure to carbon monoxide blood agents, who was initially unconscious but has regained consciousness or a casualty who shows neurological abnormalities such as dizziness, confusion, or hallucinations, has cardiac arrhythmias, bronchospasm or complains of severe headache, difficulty in breathing or chest pain. If available, breath measurement indicates that the blood carbon monoxide level exceeds 20%. 

A deterrnination that carbon monoxide might be a metaboUte of methylene chloride in humans (33) suggests that unacceptable levels of carboxyhemoglobin would exist in the blood of persons exposed to methylene chloride vapors at concentrations greater than 500 ppm for extended periods of time. These conditions are rarely encountered in most industrial appHcations. However, as with any organic solvent, adequate ventilation should be provided to ensure compliance with all industrial and governmental regulations. 

It is well known that hydrogen cyanide can be liberated during combustion of nitrogen containing polymers such as wool, silk, polyacrylonitrile, or nylons (1, 2). Several investigators have reported cyanide levels in smoke from a variety of fires (3, 4, 5). The levels reported are much below the lethal levels. Thus the role of cyanide in fire deaths would seem to be quite low. However, as early as 1966 the occurence of cyanide in the blood (above normal values) of fire victims was reported (6). Since then many investigators have reported elevated cyanide levels in fire victims (7-13). However, it has been difficult to arrive at a cyanide blood level which can be considered lethal in humans. In this report the results of cyanide analysis in blood of fire victims are reported as well as the possibility that cyanide may, in some cases, be more important than carbon monoxide as the principal toxicant in fire smoke. 

Continue oxygen therapy until patient is asymptomatic and blood carbon monoxide levels are below 10%. For individuals with blood carbon monoxide levels above 40%, consider transfer to a hyperbaric facility. 

The types of medical data that help accident investigations include (1) type and level of toxic or abusive substances in the blood, (2) location and magnitude of injuries, (3) type of poisoning (carbon monoxide, toluene, etc.), (4) signs of suffocation, (5) signs of heat exposure or heat exhaustion, and (6) signs of eye irritation. 

One of the most carefully worked out dose-response relationships is that for carbon monoxide poisoning. Based on controlled studies of exposure in humans at low levels and on observations in humans who have suffered high level exposures because of their occupation or because of accidents or suicide attempts, the relationship between blood levels of carboxyhemoglobin (COHb) and toxicity is understood as follows ... 

Therefore, when Pco = 1/220 XP02 the hemoglobin in the blood will be 50% saturated with carbon monoxide. Since air contains 21% oxygen, approximately 0.1% carbon monoxide will give this level of saturation. Hence, carbon monoxide is potentially very poisonous at low concentrations. The rate at which the arterial blood concentration of carbon monoxide reaches an equilibrium with the alveolar concentration will depend on other factors such as exercise and the efficiency of the lungs. Other factors will also affect the course of the poisoning. 

The blood of an individual exposed to carbon monoxide shows elevated levels of carboxyhemoglobin. 

Q10 Brad still has a low arterial P02. Is this likely to be related to his smoking habit Qll Suggest a reason for the high level of carbon monoxide in Brad s blood. 

The toxicological implications in the effect of the respiratory poisons on the enzyme systems of mammals are not fully comprehended, even at this stage of knowledge. For instance, Dixon and Webb (44) point out that the respiration of most animal tissues is insensitive to carbon monoxide which, in the blood, competes with oxygen for the reduced hemoproteins whereas cyanide has a broad inhibitory spectrum which includes various oxidative systems at cellular level and, most importantly, the oxidized forms of the hemoproteins, especially methemoglobin. In this latter connection, phenazine methosulfate has recently been found effective as an experimental therapeutic in cyanide poisoning of mice (13). The respiratory poisons have just been reviewed by Hewitt and Nicholas (72). 

Some of the solvent wiU be metabolized in the liver, and one product of the metabolism is the poisonous gas carbon monoxide. There have been cases of severe carbon monoxide poisoning due to prolonged exposure to methylene chloride. Someone exposed to the solvent for two to three hours may achieve a level of 15 per cent carbon monoxide in the blood, which would cause only mild effects in a healthy individual but possibly more severe problems in someone with heart or lung disease. 

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