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Arterial blood gas measurements often show that pO2 is 'normal' even though haemoglobin is bound to carbon monoxide with high affinity.

Is this because there is still oxygen bound to some subunits of the haemoglobin? Surely the CO will displace at least some oxygen, reducing the pO2? As oxygen solubility in plasma is very low, where would oxygen be in the blood if not bound to haemoglobin if there was still high pO2?

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First, let's think about what pO2 means:

pO2 is not the same as "oxygen concentration." pO2 is the partial pressure of oxygen, you can think of it as proportional to the "number of oxygen molecules per unit area leaving the solution" (or colliding with the side of the container). There is also pO2 for the atmosphere, which is going to be approximately 21% * 760mmHg = about 160 mmHg. Partial pressures are often a convenient way to measure gas concentrations, but that only works when there aren't any other interactions happening, so it's not valid for blood.

When blood comes in contact with inspired air, there are >100 mmHg of oxygen molecules hitting the solution and <100 mmHg of oxygen leaving, so there is a net diffusion of oxygen from the inspired air to the blood. If the gas in the alveoli and the blood in the lung capillaries have the same partial pressure of oxygen, there is no more net transfer of oxygen, they are at equilibrium.

Hemoglobin can't do anything to cause the blood to carry more "partial pressure" of oxygen. What hemoglobin does is to "hold on" to oxygen molecules. These "held" molecules can't leave the solution, so they don't "count" as much towards the partial pressure. Hemoglobin instead allows for a higher concentration of oxygen at the same partial pressure of oxygen. Another special thing hemoglobin does is to change its affinity for oxygen in the acidic environment of metabolically active tissue, releasing O2 at a higher partial pressure than it was initially dissolved at.

If you pumped plain saline through the lungs, it would get to about the same partial pressure of oxygen, but it wouldn't have as many oxygen molecules.

If not enough fresh air is entering the lungs, or if the air entering the lungs is low in oxygen, you would expect the blood pO2 to drop, but this isn't what happens in CO poisoning.

There is also the issue that what actually happens in CO poisoning is that affinity of hemoglobin for oxygen increases, but this is actually irrelevant to the pO2 question. The oxygen tightly bound to carboxyhemoglobin (CO-poisoned hemoglobin) doesn't "count" towards the pO2.

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    $\begingroup$ Nicely done. I added an answer with some more structure around how we measure and think about total oxygen content that may complement this. $\endgroup$ – De Novo Jan 30 at 4:29
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@Bryan's answer is good. I'd like to add a little structure around what seems to be the primary confusion in your question.

There are three important measurements here:

  1. $P_{aO_2}$
  2. $O_2$ saturation
  3. Hemoglobin concentration

$P_{aO_2}$

Arterial $P_{O2}$ ($P_{aO_2}$) is typically expressed in mm Hg. It is very specifically a measurement of the concentration of oxygen dissolved in arterial blood and NOT bound to hemoglobin. Low $P_{aO_2}$ is called hypoxemia.

$O_2$ saturation

$O_2$ saturation is a measurement of the percentage of Hemoglobin binding sites occupied by oxygen. It is expressed as a percentage, e.g., 98%.

Hemoglobin concentration

Hemoglobin concentration is a measurement of the concentration of hemoglobin protein in blood. It is typically expressed in the U.S. in g/dL.

Total oxygen content

Together, these three measurements ($P_{aO_2}$, $O_2$ saturation, and Hb concentration) determine the total oxygen content of arterial blood. Any one or any combination of these three measurements can result in hypoxia (inadequate oxygenation of tissue).

Carbon monoxide poisoning in an otherwise healthy individual is a specific cause of hypoxia that has a characteristic pattern: normal $P_{aO_2}$, normal Hemoglobin concentration, and low $O_2$ saturation. Because there is no problem breathing in oxygen or having it cross the blood gas barrier, there is a normal level of oxygen dissolved in arterial blood. $P_{aO_2}$ is normal. There is no anemia, so Hb concentration is normal. The problem is strictly a matter of $O_2$ saturation.

In many cases of hypoxia, the picture is mixed, but $CO$ poisoning is a classic example where the problem is exclusively one of $O_2$ binding. Anemia is another example. In anemia, $P_{aO_2}$ is normal, $O_2$ saturation is normal, but total oxygen content remains low because there is not enough Hemoglobin.

These are fairly complicated concepts, but covered quite well in West Respiratory Physiology, Ch. 6. The following table may be helpful. Note the footnote for $O_2$ saturation in the row for CO poisoning. Saturation is normal when calculated for Hemoglobin not bound to CO, in other words, there is nothing wrong with the Hb molecule itself. It is simply bound to something else. This is why administration of 100% $O_2$ is a useful treatment.

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  • $\begingroup$ I like the inclusion of other clinically relevant measures in your answer, +1. I think mine got to be a bit more of a ramble than I intended. Physiology is one of those things that only makes sense once you get it - and then it all clicks. I'm all for trying various ways to getting to the get it step. I'm curious about the O2 saturation measure in the presence of CO... my understanding is that arterial O2 saturation would seem normal in typical CO poisoning, because of high affinity of CO-bound hemoglobin for oxygen. $\endgroup$ – Bryan Krause Jan 30 at 4:45
  • $\begingroup$ @BryanKrause the typical bedside measurement is actually not useful in many specific cases, so this is more a physiology teaching concept. I honestly have never seen a CO poisoning patient myself, but in theory you'd have a suggestive history, normal arterial PO2 and normal Hb, and need to have some index of suspicion. Interestingly, another classic teaching about CO poisoning is that you see a cherry red complexion. It turns out, that only happens post mortem, and since we were all taught by pathologists, we passed it along for a number of years. $\endgroup$ – De Novo Jan 30 at 4:55
  • $\begingroup$ That last anecdote is both an entertaining and terrifying one. $\endgroup$ – Bryan Krause Jan 30 at 5:02
  • $\begingroup$ @DeNovo thank you. I am slightly confused when you say PaO2 is "very specifically a measurement of the concentration of oxygen dissolved in arterial blood". My understanding was that oxygen is relatively insoluble in blood (0.0031 mL / mmHg of oxygen / dL of blood), hence the need for haemoglobin. How can PaO2 therefore reach 100mmHg? Is the /mmHg term in this solubility that of the alveolar air it is exposed to that supplies the oxygen dissolving? $\endgroup$ – pincushion44 Jan 30 at 18:20
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    $\begingroup$ @pincushion44 we use partial pressure to reflect the concentration of oxygen in blood instead of mass or moles per volume because we're not interested in the mass or number of moles dissolved in arterial blood. As you understand, it is not much relative to what is bound to Hb, but O2 dissolves in blood first, before it can bind to Hb. It is important to be able to see if there is a problem getting O2 from the alveoli to the blood, or from the blood to Hb. $\endgroup$ – De Novo Jan 30 at 20:12

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