Carboxyhemoglobin (CO-Hb)

Sample

1. Collect the venous blood immediately when CO poisoning is suspected.
   1. Heparinized arterial or venous blood for spectrophotometric methodology.
   2. Because CO is rapidly cleared from the hemoglobin when the patient is exposed to fresh air.
2. Whole blood in heparin is stable >4 months infilled well-caped bottle.
3. Blood in EDTA anticoagulant is stable at room temperature for more than one week.

Precautions for Carboxyhemoglobin

1. Don’t use oxalate for the blood sample.
2. Collect the blood sample before oxygen therapy is started.
3. O₂ saturation and oximetry are inaccurate in the CO-poisoning because it measures all forms of O₂ – saturated hemoglobin and CO-Hb.

Purpose of the test (Indications) for Carboxyhemoglobin

1. This test is done to detect carbon monoxide poisoning.
2. It is prescribed for patients who are exposed to smoke inhalation, exhaust fumes, and fires.

Pathophysiology of Carboxyhemoglobin

Definition of Carboxyhemoglobin:

1. Carbon monoxide (CO) is a colorless, odorless, and tasteless gas, undetectable unless it is mixed with a visible or odorous pollutant.
2. It is produced by the incomplete combustion of such fuels as gasoline.
3. CO binds more tightly with hemoglobin than O2. It displaces the O2 and causes hypoxia.
4. CO is a chemical agent which produces hypoxic injury due to O₂ deprivation.
5. There is cherry red skin is a good clue for Carbon monoxide poisoning.

CO Poisoning mechanism:

1. CO is produced in the environment where there is partial combustion of Carbon-containing fossil fuels.
   1. Complete oxidation leads to the production of CO2.
2. Carbon monoxide combines with hemoglobin with 200 times more affinity than oxygen.
   1. CO + Hb = CO-Hb
3. CO-Hb produces a cherry-red or violet color on the skin.

4. So in the presence of CO,  there are few sites available for O2 to combine with Hb.
5. Less O2 is available for tissue respiration leads to Hypoxemia because CO-Hb cannot transport O₂.
6. CO has a high affinity for hemoglobin, almost 210 times that of oxygen.
7. CO will combine with the hemoglobin and form carboxyhemoglobin (CO-Hb).
8. Normally carboxyhemoglobin (CO-Hb) is a small fraction of the total hemoglobin <0.5%.
9. CO-Hb at a higher level leads to toxic symptoms.

10. CO poisoning is directly toxic to the intracellular oxidative mechanism and produces more nitric oxide (NO).
11. When CO poisoning takes place, ask for Hb analysis for CO-Hb.
12. CO is readily cleared by breathing normal air.
13. Fetal Hb has more affinity for CO, and if these fetuses are exposed to CO, they are more at risk.

Sources of carbon monoxide (CO) are:

1. Newborn where the fetal Hb breakdown yields endogenous CO.
2. Tobacco smoke.
3. Automobile exhaust fumes.
4. Natural gas heaters where there is less ventilation.
5. Industrial pollution like:
   1. Coal gas.
   2. Charcoal burning.
   3. Tobacco smoke.
6. Defective gas stoves.
7. Petroleum and natural gas fuel fumes.
8. Endogenous production of the CO:
   1. It is produced from the heme, and the CO-Hb level is ≥1% ( 0.2% to 0.8%).
   2. It is increased in hemolytic anemia and smokers.
   3. Bleeding in the intestine.
      1. In smokers, it may vary from 4% to 20%.
      2. In the case of smokers exposed to CO may have CO-Hb of around 10%.
   4. CO is also produced in the liver by metabolizing dichloromethane (methyl chloride), which is found in paints and varnish.
9. People  who are prone to get CO-poisoning:
   1. In defective furnaces.
   2. A worker such as coal mining.
   3. The firefighter.
   4. Smokers of cigarettes, cigars, or pipes in the closed space.
   5. Accidental poisoning was most often seen in house fires, engine exhaust (car left starting in the closed garage), indoor heaters, and stoves.
   6. Unventilated spaces where charcoal and gas are burning are the source of poisoning during winter power outages.
10. Intentional CO-poisoning is common in suicide cases.
11. The half-life of elimination of CO is about 4 hours for a person breathing atmospheric air.
    1. But for smokers, this level may remain high.

Signs and symptoms of Carbon monoxide poisoning:

1. The brain and the heart are more prone to be affected by CO.
2. Chronic exposure to CO may lead to polycythemia.
3. CO-Hb produces cherry-red color on the blood and skin.
4. There is a direct relationship between CO and symptoms of heart disease, angina, and myocardial infarction.
5. This CO poisoning occurs from the house fire, gas heaters, stoves, and engine exhaust.
   1. 30% to 40% of carboxyhemoglobin contents are associated with severe symptoms.
   2. >50% is associated with coma.
   3. Cigarette smoking may produce levels as high as 10% to 15%.
6. There are nausea and weakness.
7. There is a headache, dizziness, and vomiting.
8. Tinnitus is ringing in the ears.
9. It upsets the stomach.
10. The patient may have chest pain.
11. The patient will be confused.
12. Drunk or sleeping people may die due to CO poisoning.

Carbon monoxide % level effects on the body:

CO level	Clinical presentation of the patient
0.4% to 2%	Normal (nonsmoker person)
2% to 6%	Normal smoker
10% to 20%	Headache Dyspnea on exertion Mild symptoms
20% to 50%	Severe symptoms Lethargy Headache Loss of consciousness
>50%	The patient will go into a coma Ultimately there is death

Various levels of CO% and clinical effects on the body:

CO-saturated Hb %	Signs and Symptoms
10	Slight dyspnoea
20	A headache
30	Irritable, impaired judgment, Loss of memory
40	Confusion, decreased vision, weakness
50	Fainting, ataxia, and collapse
60	Coma
> 60    (>70%)	death

Symptoms are correlated with % of carbon monoxide (CO) poisoning:

CO-Hb %	Clinical presentation
0% to 2%	Patients are asymptomatic
2% to 5%	It is seen in moderate smokers Patients are usually symptomatic There may be effects on the orientation
5% to 10%	It is seen in heavy smokers There is slight dyspnoea on mild exertion
10% to 20%	There is a mild headache There is moderate dyspnoea on moderate exertion
20% to 30%	There is a marked headache The Patient is irritable There is easy fatigability There is disturbing memory There is an impairment of the judgment and vision
30% to 40%	There is a severe headache The patient is confused and dizzy The patient has weakness and nausea There is decreased vision
40% to 50%	There is a severe headache The patient is confused and fainted The patient may have hyperventilation Ultimately patient may collapse There is ataxia
50% to 60%	The patient will go into a coma The patient will have intermittent convulsions
>60%	There is hypotension Respiratory failure Death will occur if the exposure to CO is continued
80%	It is a rapidly fatal state End is death Death may occur even at a low level of 20%

Measurement (Lab diagnosis) of CO poisoning:

1. For CO estimation, can use venous or arterial blood.
2. CO is measured by CO-oximeter.
3. A blood gas analyzer measures oxyhemoglobin by calculation.
4. Lactate can be measured.
5. Calculation of the anion gap.
6. Check myocardial markers.

The normal level of carboxyhemoglobin

Source 1

• CO-Hb = <0.5% of total hemoglobin.
• Newborn = upto 5 % saturation of total Hb.
• Nonsmoker = <3 % saturation of total Hb.
  • Smoker Light = 2 to 5 % saturation of total Hb.
  • Smoker heavy = 5 to 10 % saturation of total Hb.
• Critical value = >20 % saturation of total Hb.
• Lethal value   =  >50 % saturation of Hb.

Source 2

Clinical condition	% saturation of Hb
Nonsmokers	0.5 to 1.5
Smokers
1 to 2 packs /day	4 to 5
>2 packs/day  (heavy smoker)	8 to 9
Toxic level
Toxic level	>20
Lethal level	>50

Source 3

Saturation of hemoglobin

• Nonsmoker = <3%
• Smoker = ≤ 12%
• Newborn = ≥ 12%

Source 2

Clinical values and their effects:

COHb %	Clinical signs and symptoms
20 to 30%	Dizziness, headache,  and disturbance in judgment
30 to 40%	Tachycardia, hyperpnea, hypotension, and confusion
50  to 60%	Coma
>60%	Death

Source 4

• Nonsmoker = <2% of total Hb.
• Light smoker = 4 to 5% of total Hb.
• Heavy smoker = 6 to 8% of total Hb.
• Newborn = 10 to 12% of the total Hb.

Another source

• Smoker = 2.1% to 4.2%
• Nonsmoker = <2.3%

Increased level of CO:

• This is 50 to 60% seen in CO poisoning.

Lab findings in CO- poisoning:

1. Whole blood with heparin or EDTA as an anticoagulant is used.
   1. The specimen should be mixed thoroughly before performing the test.
2. Blood pH is decreased, leading to metabolic acidosis due to tissue hypoxia.
3. Arteria Oxygen (pO₂) is normal. Oxygen (O) is markedly decreased.
4. Arterial pCO2 may be normal or slightly decreased.
5. Confirm the CO in the exhaled breath.

Treatment:

1. CO- toxicity needs a high concentration of O₂ to replace the CO-Hb.
2. In the case of severe CO, toxicity may be treated with hyperbaric oxygen (100% O2 gas).

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