Carbon monoxide (CO) poisoning, whether intentional or accidental, occurs when one inhales the colorless and odorless carbon monoxide gas. Despite improved awareness and sensory alarms, multiple deaths occur each year.

CO binds to hemoglobin with 200 times the affinity of oxygen. CO also shifts the oxygen dissociation curve to the left (the Haldane effect), which decreases oxygen release to tissues. CO can also bind cytochrome oxidase aa3/C and myoglobin. Reperfusion injury can occur when free radicals and lipid peroxidation are produced.

The treatment of CO poisoning with hyperbaric oxygen therapy (HBOT) is based upon the theory that oxygen competitively displaces CO from hemoglobin. While breathing room air, this process takes about 300 minutes. While on a 100% oxygen nonrebreather mask, this time is reduced to about 90 minutes; with HBOT, the time is shortened to 32 minutes. HBOT (but not normobaric oxygen) restores cytochrome oxidase aa3/Cand helps to prevent lipid peroxidation. HBOT is also used to help prevent the delayed neurologic sequelae (DNS); treatment instituted sooner is more effective.Multiple papers describe controversial methods and conclusions about the use of HBOT for CO poisoning.

Patients with CO poisoning can present with myriad symptoms that they may not initially attribute to CO poisoning, as CO is considered the “great imitator” of other illnesses.Presentation can include flulike symptoms such as headache, visual changes, dizziness, and nausea. More serious manifestations include loss of consciousness, seizures, chest pain, ECG changes, tachycardia, and mild to severe acidosis.

Candidates for HBOT are those who present with morbidity and mortality risks that include pregnancy and cardiovascular dysfunction and those who manifest signs of serious intoxication, such as unconsciousness (no matter how long a period), neurologic signs, or severe acidosis. CO-hemoglobin (Hgb) level usually does not correlate well with symptoms or outcome; many patients with CO-Hgb levels of 25-30% are treated.

Pregnant females often have a CO level that is 10-15% lower than the fetus. Fetal Hgb not only has a higher affinity for CO but also has a left-shifted oxygen dissociation curve compared with adult hemoglobin. Exposure to CO causes an even farther leftward shift, in both adult and fetal hemoglobin, and decreased oxygen release from maternal blood to fetal blood and from fetal blood to fetal tissues. Pregnant patients with CO-Hgb levels greater than 10% should be treated with HBOT.

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