Carbon monoxide (CO) is a colorless, odorless, and tasteless gas produced by the incomplete combustion of carbon-containing fuels. Hemoglobin, a protein within red blood cells, serves as the body’s primary transporter of oxygen. This article explains how carbon monoxide interferes with oxygen transport.
Hemoglobin’s Normal Function
Hemoglobin is a protein within red blood cells, responsible for delivering oxygen from the lungs to tissues and organs. Each hemoglobin molecule contains four subunits, each holding a heme group, an iron-containing structure. Oxygen molecules bind reversibly to the iron atom within these heme groups in the lungs, where oxygen concentration is high.
Upon reaching tissues with lower oxygen levels, hemoglobin releases the bound oxygen, allowing it to diffuse into cells for metabolic processes. This reversible binding and release ensures a continuous oxygen supply for cellular respiration and organ function.
How Carbon Monoxide Binds to Hemoglobin
Carbon monoxide interferes with oxygen transport by binding directly to hemoglobin. Its affinity for hemoglobin is significantly greater than oxygen’s, estimated at 200 to 250 times stronger. This means even small CO concentrations can readily displace oxygen from hemoglobin.
When carbon monoxide binds to the iron atom in the heme group, it forms a stable compound called carboxyhemoglobin (COHb). This binding occurs at the same sites where oxygen would normally attach, occupying these positions and preventing oxygen from binding. While CO binding to hemoglobin is reversible, its strong affinity means CO molecules remain attached for a prolonged period. The formation of COHb significantly reduces the blood’s capacity to carry oxygen, leading to oxygen deprivation in tissues.
The Body’s Response to Carbon Monoxide Binding
The formation of carboxyhemoglobin (COHb) directly impacts the body’s ability to deliver oxygen, leading to hypoxia. When hemoglobin molecules are occupied by carbon monoxide, fewer sites are available for oxygen binding, resulting in less oxygen transported to tissues. This effect is pronounced in organs with high oxygen demands, such as the brain and heart.
Reduced oxygen supply to the brain can cause symptoms like headache, dizziness, and confusion, as neuronal function is impaired. The heart, which relies heavily on a constant oxygen supply for pumping blood, may experience strain or irregular rhythms. As COHb levels increase, symptoms can worsen, progressing to nausea, vomiting, fatigue, and even loss of consciousness or seizures. Severe or prolonged oxygen deprivation can lead to widespread organ damage and be fatal.
Recognizing and Treating Carbon Monoxide Poisoning
Diagnosing carbon monoxide poisoning involves a blood test to measure the percentage of carboxyhemoglobin (COHb). This measurement directly indicates the extent to which hemoglobin has been saturated with carbon monoxide. Prompt diagnosis is important because symptoms often mimic other common illnesses, making initial recognition challenging.
The main treatment for carbon monoxide poisoning is administering 100% oxygen through a non-rebreather mask. This high concentration of oxygen helps displace carbon monoxide from hemoglobin, facilitating its removal. For severe poisoning, such as with neurological symptoms or high COHb levels, hyperbaric oxygen therapy may be used. This treatment involves breathing 100% oxygen in a pressurized chamber, increasing dissolved oxygen in the blood and accelerating CO elimination. If carbon monoxide poisoning is suspected, evacuate to fresh air immediately and seek urgent medical attention.