CO Poisoning Question

[Akimbo]

This quiz reminded me of a question that has been lurking in the back of my mind for years. The layman's description of CO Poisoning explains that hemoglobin has a higher affinity for CO, which crowds out Oxygen molecules. Got it.

1. So how does increasing the PPO2 during CO treatment change that affinity?
2. Also, where do the CO molecules go when the hemoglobin lets loose of them (out through the lungs or some other exit)?
3. Is there a defined threshold where the PPO2 is enough to reverse the process?

 

[Zef]

There is a bit more going on with CO poisoning than just the bond between CO and hemoglobin, but here is a simplistic explanation on what is going on in the body:

When CO is inhaled one of the things that happens is it forms carboxyhemoglobin in the red blood cells. The half-life of this bond is cited as approximately 320 minutes when breathing air, 74 minutes when breathing 100 O2 and further decreased to 23 minutes when 100 O2 is coupled with hyperbaric treatment at 3 ATA. The 100 O2 hyperbaric therapy dramatically reduces the half-life of caboxyhemoglobin and significantly aids the body's ability to regain normal O2 levels. As the bonds that bind the CO to the hemoglobin break down some CO is exhaled and the rest is broken down by oxidative metabolism and then filtered from the blood and otherwise eliminated from the body.

Here is an article that has some details:
Hyperbaric Treatment Of Carbon Monoxide Toxicity - StatPearls - NCBI Bookshelf

"The mechanism of action of HBO2 is not only to cause more rapid displacement of the CO from hemoglobin and generate normal oxyhemoglobin in the red blood cell, but the oxygen delivery to the tissue is also increased by the oxygen that is dissolved in the plasma. The other benefit of the HBO2 is to reduce the adherence of neutrophils on the damaged endothelium of the blood vessels in the brain, which reduces tissue edema and reduces the lipid peroxidation. The extra oxygen that is delivered to the tissue also helps to reduce the CO bound to the cytochrome proteins in the mitochondria of the cells and contributes to restoring oxidative phosphorylation, which neurons are especially dependent upon for normal function and survival from the ischemic insult."

Carbon monoxide poisoning

"The mainstay of treatment is 100% oxygen administration until the carboxyhaemoglobin level is normal. On this regimen the half-life of carboxyhaemoglobin is 74 minutes (compared with 320 minutes breathing air)16, 23. Lactic acidosis facilitates tissue oxygen diffusion and should not be corrected unless extreme (pH<7.15)."

and

"Hyperbaric oxygen has many benefits. The half-life of carboxyhaemoglobin at 3 ATA (absolute atmospheres) of oxygen is only 23 minutes27. Other benefits are improved mitochondrial function, impairment of platelet adhesion in the capillaries and inhibition of lipid peroxidation"

Another good resource: https://www.atsdr.cdc.gov/ToxProfiles/tp201-c2.pdf

-Z

 

[fmerkel]

1. It's simple competition for binding on the Hb. The O2 and CO molecules are constantly binding and letting go. When you up the PPO2 you essentially send a 'mob' of aggressive O2 in to compete.
2. Once loose it passes out of the lungs.
3. No defined 'threshold'. It happens at sea level but slowly, meaning a seriously affected person dies before enough HB is set free to allow sufficient O2 into the body. As the PP02 goes up 2 things happen:
- The competition as described in #1.
- There is also O2 dissolved in the plasma. At sea level the amount is negligible, not contributing much to support life. At higher pressure, not just higher %, the dissolved component can become high enough to sustain life, while the O2 vs CO struggle is going on to free up Hb. That's why getting these people into hyperbarics + high %O2 becomes critical if they've taken on too much CO.

Interesting note - a single cigarette can raise CO levels in the blood 10-15%.
Since finger oximeters do NOT measure actual O2 content in the blood this will not show up on an oximeter. Oximeters measure the color RED. Oxygenated Hb is 'redder' than de-oxygenated Hb.
CO+Hb is EVEN REDDER, so a person can literally be dying of CO poison and an oximeter will show they are just fine, excellent even.

 

[Akimbo]

That's why getting these people into hyperbarics becomes critical.

Unfortunately, HBOT chambers are not as widely distributed as CO poisoning. Most places are stuck with an Oxygen mask and hoping it is enough unless there is some new drug to help.

 

[BrackaFish]

Unfortunately, HBOT chambers are not as widely distributed as CO poisoning. Most places are stuck with an Oxygen mask and hoping it is enough unless there is some new drug to help.

The outcome in a hospital setting is usually better than slap on an O2 mask and pray. Because of the time involved in getting a patient to a chamber and the fact that the issue is usually resolved within an hour, patients are better off in a hospital setting. Life support including drugs, mechanical ventilation including higher PEEP levels and qualified staff will usually keep a patient alive until the CO is washed out. Also medical care is sometimes difficult in a single place chamber. However, as a diver, I do agree that we need more chambers.

 

[Akimbo]

The outcome in a hospital setting is usually better than slap on an O2 mask and pray.

I was operating under the assumption that an EMT will get an O2 mask on the victim long before a patient gets to a hospital or HBOT chamber; or even in the ambulance. Fortunately (for the victim) the cherry red fingernails and lips make CO poisoning a pretty safe guess. It's hard to imagine that ERs get very many walk-in cases.

All things being equal, I wish there was a chamber in my area. :sigh:

 

[Storker]

So how does increasing the PPO2 during CO treatment change that affinity?

It doesn't change the affinity.

The bonding of CO vs O2 to hemoglobin is governed by the respective affinities. CO has a higher affinity, but given enough O2 the CO will be out-competed. The affinity (probability of bonding vs amount) is the same, but since there's so much more O2 the O2 will out-compete the CO.

 

[Storker]

I was operating under the assumption that an EMT will get an O2 mask on the victim long before a patient gets to a hospital or HBOT chamber

If you don't have the patient in a chamber, you do whatever you can to increase the pPO2. Before you arrive at the chamber, the best you can do is to put the patient on 100% O2.

 

[Akimbo]

If you don't have the patient in a chamber, you do whatever you can to increase the pPO2. Before you arrive at the chamber, the best you can do is to put the patient on 100% O2.

Also true for DCS treatment and many other medical maladies. You do the best you can with the what you've got.

 

[Zef]

It doesn't change the affinity.

The bonding of CO vs O2 to hemoglobin is governed by the respective affinities. CO has a higher affinity, but given enough O2 the CO will be out-competed. The affinity (probability of bonding vs amount) is the same, but since there's so much more O2 the O2 will out-compete the CO.

I am not sure the literature on the subject supports what you are asserting. In a CO poisoning situation the CO is already bonded to the red blood cells by the time treatment occurs if it occurs. I don't think there is competition between O2 and the CO, especially given that CO is said to have 210 times the affinity for hemoglobin than O2 and it has an even stronger affinity for myoglobin. The higher affinity means greater probability of bonding and less likely to be displaced. My understanding is that the presence of O2 does not displace the CO but accelerates the breakdown of the bonds between the hemoglobin and the CO molecules. The accelerated half-life increases the washout of the CO from the blood making the hemoglobin available for binding with the O2 molecules. This happens naturally at a much slower rate without the presence of supplementary O2 treatment, and the effect is increased as the PPO2 is increased via hyperbaric treatment coupled with the O2.

What I am unsure about is what the specific effect O2 has on the CO-Hemoglobin bond...perhaps it shifts the Ph balance resulting in an icnreased oxidative metabolic effect, but according to the literature that accounts for a small percent of CO elimination. Perhaps the increased presence of O2 reduces the half-life of CO in the blood not by displacing it but by converting the CO to CO2 and then eliminating it through exhalation. The literature mentions that a greater amount of CO is eliminated through exhalation but I coud only find one source (the last one listed below) that gave much indication of the actual mechanism for this.

https://www.who.int/ipcs/publications/ehc/ehc_213_part_3.pdf?ua=1
Carbon monoxide poisoning.
20.4 Transport of Gases in Human Bodily Fluids – Concepts of Biology – 1st Canadian Edition
Carbon monoxide poisoning.
https://www.atsdr.cdc.gov/ToxProfiles/tp201-c2.pdf
https://journals.physiology.org/doi/abs/10.1152/ajplegacy.1969.217.2.354?journalCode=ajplegacy

-Z