Scientia et Arte

If science were art and art were science, then the howling black wolf has probably swallowed some N-(4-hydroxyphenyl)ethanamide.

Carbon Monoxide Poisoning

In November of 2011, a 68-year old woman, Mrs. S., complained of headaches occurring at irregular intervals for the past three days. She also took ibuprofen every 8 hours for the past 2 days but the symptoms did not abate. Her other symptoms included shortness of breath, dizziness, weakness, and chest pains at irregular intervals. However, it is interesting to note that she “felt better” when she went out to shop. It seems her headaches started after she turned on the heating system. Furthermore, her son and his wife lived on the second floor apartment above hers and had symptoms similar to hers. They did not travel recently nor were they in contact with persons who had infections. Vital signs and laboratory test results were relatively normal for a woman of her age except that her carboxyhemoglobin (COHb) level was 20% (less than 10% is normal).

The case just recounted is a typical scenario of carbon monoxide poisoning (CO poisoning) and the elevated levels of COHb in her blood was a tell-tale sign, at least in a laboratory. One reason why CO poisoning is deadly is not so much due to CO’s sheer toxicity but because it’s so subtle and easily ignored. As CO is colorless, tasteless, and odourless; symptoms of CO poisoning are sometimes mistaken to be due to somethings else like how Mrs. S. dismissed her poisoning as a mere headache at first. Furthermore, other individuals were also put at risk unknowingly. The symptoms are thus easily confused for flu, depression, food poisoning or gastroenteritis for children. Note that pregnant women are especially susceptible since CO causes growth retardation, fetal distress or even death to the unborn – even survivors of the poisoning might exhibit developmental disorders and brain damage.

Normally, the first oxygen binding to haemoglobin (Hb) would change its confirmation to allow easier binding of subsequent oxygens; however, it is relatively more difficult for the first oxygen to bind with oxygen in the first place. This characteristic allows haemoglobin to be a good oxygen transporter: binds oxygen when oxygen pressure is high like in the lungs, but easily lets it go when the pressure is low like in the tissue. CO poisoning first occurs when CO is inhaled and binds to one of hemoglobin’s oxygen binding sites to form the compound COHb complex. Counter-intuitively, the CO actually increases the Hb’s capacity to bind oxygen, changing the s-like binding capacity versus oxygen pressure graph to a consistently hyperbolic shape where binding capacity is relatively high even at lower pressures – resulting to the COHb being unable to deliver the oxygen molecules to the tissues since the oxygen molecules bind too strongly to the COHb to be released. Furthermore, CO binds more readily to Hb than oxygen (about 210 times more readily) hence increased levels of CO in the atmosphere effectively decrease the fraction of Hb capable of performing its functions.

The curve on the right is the usual behavior for Hb and on the left is the curve for CO poisoned Hb. At lower pressures in tissue (to the left side of both curves), poisoned Hb exhibitis higher oxygen binding capacity – the Hb cannot deliver oxygen to tissue/

The specific mechanisms of how CO is multifaceted, complex, and sometimes little understood but it generally involves the deprivation of oxygen from tissue (or hypoxia, more technically). Binding of CO to cardiac myoglobin for example causes irregular heart rhythm, low blood pressure, and myocardial depression. The disrupted functioning of the heart, in turn, causes further disruption which eventually leads to cardiac hypoxia and then death – often the cause of death of poisoned individuals. Hypoxia in other tissues usually results in the precipitation of endothelial cells and the platelet generation of nitric oxide which further react to form highly reactive peroxynitrates. This free radical in the brain causes mitochondrial dysfunction, capillary leakage, and cell death with the end result being the degradation of lipids and fatty acids in the brain, specifically myelin.

Poisoning is usually treated with the inhalation of high pressure oxygen. Since the CO binds competitively to the active site of the Hb tetramer, the condition might be alleviated by introducing high concentrations of oxygen to “bugger off” the CO molecules from taking oxygen’s rightful place. Preventing the condition can also be done by being wary of burning hydrocarbons and regularly checking central heating systems.

References:

Gorman DDrewry AHuang YLSames C (2003). “The clinical toxicology of carbon monoxide.” Toxicology 187(1): 25-38.

Olson KR (1984). “Carbon monoxide poisoning: mechanisms, presentation, and controversies in management. Journal of Emergency Medicine 1(3):233-43.

Ivan Blumenthal (2001). “Carbon monoxide poisoning.” Journal of the Royal Society of Medicine  94(6): 270–272.

Ruth-Sahd LA, Zulkosky K, Fetter, ME (2011). “Carbon Monoxide Poisoning: Case Studies and Review.” Dimensions of Critical Care Nursing 30(6): 303-314.

Image Sources:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1281520/figure/fig1/

 

[Post by Deo Mostrales]

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This entry was posted on October 1, 2012 by in Medical Curiosities and tagged , .
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