What is the primary consequence of carbon monoxide poisoning on hemoglobin?

The primary consequence of carbon monoxide poisoning on hemoglobin is a reduction in the oxygen-carrying capacity. Carbon monoxide (CO) binds to hemoglobin with a much higher affinity than oxygen, effectively competing with oxygen for binding sites. When CO binds to hemoglobin, it forms carboxyhemoglobin, which prevents hemoglobin from transporting oxygen throughout the body. As a result, the amount of oxygen available to tissues is severely diminished, leading to hypoxia and subsequent cellular damage.

This condition does not inherently cause an increase in blood volume, a decrease in heart rate, or an elevation in blood pressure. While secondary physiological responses may occur due to the diminished oxygen delivery—such as an increase in heart rate or changes in blood pressure—the direct and primary impact of carbon monoxide poisoning is the reduced capacity of hemoglobin to carry oxygen. Understanding this mechanism is essential for recognizing the dangers of carbon monoxide exposure and its effects on body function.