Carbon monoxide hypoxia caused

Toxicology. Carbon monoxide (CO) causes tissue hypoxia by preventing the blood from carrying sufficient oxygen. 

The nervous system is vulnerable to attack from several directions. Neurons do not divide, and, therefore, death of a neuron always causes a permanent loss of a cell. The brain has a high demand for oxy gen. Lack of oxygen (hypoxia) rapidly causes brain damage. This manifests itself both on neurons and oligodendroglial cells. Anoxic brain damage may result from acute carbon monoxide, cyanide, and hydrogen sulfide poisonings. Carbon monoxide may also be formed in situ in the metabolism of dichloromethylene. 

The model of carbon monoxide toxicity proposed by Kao and Nanagas (2006) combines the cascade of changes resulting from three primary events - binding to HB, direct cellular injury, and increased NO activity. CO is not a radical but many of the injuries produced by it are those that are caused by oxidative stress, which is secondary to hypoxia. In the model of Kao and Nanagas (2006), the oxidant is NO, which contributes to oxidative damage to the brain and produces the clinical syndrome of delayed neurologic sequelae (Thom et al, 1997). 

Carbon monoxide and methemoglobin-forming agents interfere with oxygen transport, resulting in cellular hypoxia. Cyanide interferes with oxygen use and therefore causes an apparent cellular hypoxia. 

Effects Carbon monoxide causes tissue hypoxia. Headache is one of the first symptoms, followed by confusion, decreased visual acuity, tachycardia, syncope, coma, convulsions, and death. Collapse and syncope occur when approximately 40% of hemoglobin has been converted to carboxyhemoglobin. These adverse effects may be aggravated by high ambient temperature and high altitude. 

Chemical asphyxiates are toxic agents which enter into reactions to cause histotoxic hypoxia. These chemicals prevent the red blood cells from carrying oxygen. Some more familiar chemical asphyxiates are carbon monoxide, nitrites, hydrogen sulhde, and aniline. 

Tumor-associated or therapy-induced anemia can lead to a reduced O2 transport capacity of the blood, a major (systemic) factor contributing to the development of hypoxia (anemic hypoxia). This type of hypoxia is especially pronounced in tumors or tumor areas exhibiting low perfusion rates. A. similar condition can be caused by carboxyhemoglobin (HbCO) formation in heavy smokers, which leads to a functional anemia, since hemoglobin blocked by carbon monoxide (CO) is no longer capable of transporting oxygen. 

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