Carbon Monoxide Poisoning Article Index for
Carbon Monoxide
Website Links For
Carbon
 

Information About

Carbon Monoxide Poisoning




  Name Carbon monoxide poisoning
  ICD10 T58
  ICD9


Carbon Monoxide poisoning is a form of toxicity due to two main mechanisms:
  • CO binds to Hemoglobin and decreases the oxygen content of blood; this results in acute tissue hypoxic injury

  • CO binds to Mitochondrial Cytochrome Oxidase and impairs oxidative phosphorylation and causes cell damage


Carbon Monoxide (CO) binds very strongly to the Iron Atom s in Hemoglobin , the principal Oxygen -carrying compound in Blood . The affinity between CO and hemoglobin is 240 times stronger than the affinity between hemoglobin and oxygen.


ACUTE HYPOXIC INJURY DUE TO CARBOXYHEMOGLOBIN

CO binds to the hemoglobin, producing Carboxyhemoglobin (HbCO), and blocks these sites on hemoglobin where oxygen would normally bind. The reduction in oxygen carrying capacity of the blood results in acute tissue Hypoxia . An additional factor impairing oxygen release to the tissues is the left shift of the oxyhemoglobin dissociation curve that occurs due to CO.

A sufficient exposure to carbon monoxide can reduce the amount of oxygen taken up by the brain to the point that the victim becomes unconscious, and can suffer brain damage or even death from Anoxia . The brain regulates breathing based upon carbon dioxide levels in the blood, rather than oxygen, so a victim can succumb to anoxia without ever noticing anything up to the point of collapse. Hemoglobin acquires a bright red colour when converted to carboxyhemoglobin, so a casualty of CO poisoning is described in textbooks as looking pink-cheeked and healthy. However, this "classic" cherry-red appearance is very uncommon -- it has only been noted in 2% of cases -- so care should be taken not to overlook the diagnosis even if this colour is not present.

Fetal Hemoglobin has an even higher affinity for CO than adult hemoglobin. HbCO also takes longer to clear from the fetal circulation. Mothers who seem to have only moderate CO poisoning may consequently have a fetus which is very severely damaged.


DELAYED NEUROLOGIC DAMAGE DUE TO MITOCHONDRIAL DAMAGE

People who survive an acute episode of severe poisoning often (14-40% of cases) develop delayed neurological dysfunction. The level of COHb in the blood does not correlate very closely with symptoms or with outcome and cannot explain the phenomenon of delayed neurologic sequelae.

The mechanism for the delayed neurologic injury is due to the adverse effects of the intracellular uptake of Carbon Monoxide . CO binds to the mitochondrial enzyme Cytochrome Oxidase , impairing Oxidative Phosphorylation and causes oxidative stress in the cell. Additionally, nitric oxide released from Platelets and endothelial cells leads to formation of the free radical Peroxynitrite which further damages Neurones , and the vascular Endothelium of the cerebral vessels. Consequently, Lipid Peroxidation occurs in the brain during 'recovery' from the acute CO poisoning. The injury results also in an increased release of the excitatory Neurotransmitter Glutamate which causes further damage in the brain. The result is cognitive defects (especially affecting memory and learning) and movement disorders. The movement disorders are related to a predilection of CO to damage the Basal Ganglia .

These delayed neurological effects may develop over days following the initial acute CO poisoning.

With chronic low-level exposure, similar neurologic injury may occur. Carbon monoxide acts as a potent neurotoxin, creating irreversible lesions in the brain's white matter (i.e., the Myelin sheath). Such lesions, which are similar to those found in multiple sclerosis, can result in severe cognitive impairment.


PARTICULAR RISK SITUATIONS

A major problem of accidental CO poisoning that still exists is the use of heaters, particularly gas water heaters and gas fires which are improperly vented. A number of deaths occur every year from this cause. This can occur in any enclosed area with such a heater: a home, a with an obstructed Chimney , burning Charcoal indoors, etc. A Carbon Monoxide Detector can be set up in homes (and other enclosed spaces with heaters) to detect a build-up of CO. If a high level of CO is detected, the detector sounds an alarm, giving people in the area a chance to ventilate the area or safely leave the building before they succumb to anoxia.

CO poisoning can occur in Scuba diving due to faulty or badly sited Diving Air Compressor s. See under Effects Of Relying On Breathing Equipment While Underwater for more information. At great depth pressure, enough oxygen to support life may dissolve in the Blood Plasma and thus bypass the blocked hemoglobin; the CO poisoning symptoms show when the diver comes back up to a shallower depth.

First Aid for carbon monoxide poisoning is to immediately remove the victim from the exposure without endangering oneself, Call For Help , apply CPR if needed and provide 100% oxygen by a tight fitting Oxygen Mask . Hyperbaric Oxygen Therapy is a treatment for carbon monoxide poisoning but its efficacy has not been clearly established. Part of the problem is the often long delays between time of poisoning and the time the patient finally enters the chamber.


PHYSIOLOGICAL ROLE

Carbon monoxide is produced naturally by the body. The breakdown-product of Hemoglobin , heme, is a substrate for the enzyme Heme Oxygenase which produces CO and Biliverdin . This is the only reaction in the body which produces CO.

The biliverdin is converted to Bilirubin by Biliverdin Reductase in macrophages of the Reticuloendothelial System . The lipid soluble unconjugated bilirubin is transported in the blood bound to Albumin , taken up by the Hepatocytes , conjugated with glucuronic acid and transported into the bile canaliculi for excretion from the body.

The endogenously produced CO may have important physiological roles in the body (eg as a Neurotransmitter ).


SOCIOLOGICAL NOTES

As the availability of other Poison s such as Cyanide and Arsenic was placed under more and more stringent legal restrictions, the carbon monoxide in Town Gas became the principal method of Suicide by poisoning. Later, suicide was often committed by inhaling Exhaust fumes of running engines. Air-quality regulations have begun to reduce suicide by this route, as Catalytic Converters were designed to clean up the exhausts and remove all but a trace of CO.

As entry, which includes an extensive discussion of “Internet Suicide Pacts”.)

The nature of CO poisoning can be stressful on mourning relatives:
  • CO kills quickly and without much warning. It is possible for CO to kill multiple family members overnight.

  • CO can kill family pets as well.

  • One may feel guilt/sadness because the death(s) may have been completely prevented if someone had only set up a Carbon Monoxide Detector earlier.



SEE ALSO

Carbon Dioxide Poisoning


RESOURCES