Carbon Monoxide Poisoning

Why is arterial pO2 normal in carbon monoxide poisoning?

In carbon monoxide (CO) poisoning, the arterial partial pressure of oxygen (pO2) can appear normal or near-normal, which is often referred to as “cherry-red” blood syndrome. This is rather paradoxical since CO is known to bind tightly to hemoglobin, reducing its ability to transport oxygen. The reason for this normal pO2 is due to the specific way carbon monoxide interacts with hemoglobin in the blood.

When CO is inhaled, it competes with oxygen for the binding sites on hemoglobin. However, carbon monoxide has a much higher affinity for hemoglobin than oxygen, meaning it binds more readily and strongly. Consequently, hemoglobin has a greater affinity for CO over oxygen, forming carboxyhemoglobin (COHb). When COHb is formed, it effectively reduces the availability of binding sites for oxygen.

In a normal healthy individual, the oxygen-carrying capacity of hemoglobin is nearly saturated at all times. The normal pO2 level in arterial blood typically reflects the equilibrium between oxygen dissociating from hemoglobin and oxygen binding to it. However, in carbon monoxide poisoning, the affinity between CO and hemoglobin is significantly greater than that between oxygen and hemoglobin.

As a result, even though there is a decreased amount of oxygen carried by the hemoglobin due to CO binding, the remaining oxygen that is still unbound can maintain a relatively normal pO2 level in arterial blood. This can be misleading as the body cells may still suffer from oxygen deprivation.

In summary, in carbon monoxide poisoning, the arterial pO2 can be normal or near-normal due to the displacement of oxygen by carbon monoxide on hemoglobin. This phenomenon is attributed to the higher affinity of CO for hemoglobin, allowing some oxygen to remain unbound and maintain a normal pO2 level despite reduced oxygen delivery to tissues.

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