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Understanding Carbon Monoxide Poisoning

Carbon monoxide is an odorless, colorless gas produced by incomplete combustion that can cause both acute and chronic poisoning. It is the leading cause of accidental poisoning deaths in the United States, accounting for over 50,000 emergency room visits and 6,000 accidental deaths per year. Carbon monoxide binds to hemoglobin in red blood cells over 200 times more strongly than oxygen, preventing oxygen from being distributed throughout the body and causing hypoxia. Symptoms of carbon monoxide poisoning range from mild headaches and nausea to seizures, loss of consciousness, and death. Treatment focuses on removing the victim from the contaminated area and administering hyperbaric oxygen therapy to accelerate the removal of carbon monoxide from hemoglobin.

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Ioana Cozma
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65 views14 pages

Understanding Carbon Monoxide Poisoning

Carbon monoxide is an odorless, colorless gas produced by incomplete combustion that can cause both acute and chronic poisoning. It is the leading cause of accidental poisoning deaths in the United States, accounting for over 50,000 emergency room visits and 6,000 accidental deaths per year. Carbon monoxide binds to hemoglobin in red blood cells over 200 times more strongly than oxygen, preventing oxygen from being distributed throughout the body and causing hypoxia. Symptoms of carbon monoxide poisoning range from mild headaches and nausea to seizures, loss of consciousness, and death. Treatment focuses on removing the victim from the contaminated area and administering hyperbaric oxygen therapy to accelerate the removal of carbon monoxide from hemoglobin.

Uploaded by

Ioana Cozma
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We take content rights seriously. If you suspect this is your content, claim it here.
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Hygiene Personal Presentation

Carbon Monoxide Poisoning Ioana Cozma


Year 3 Medical Student
“The silent killer” Carol Davila University
Background
❖ Carbon monoxide is a gas that is:
❖ Colourless
❖ Odourless
❖ Non-irritating
❖ Lighter than air
❖ Produced by incomplete combustion of carbonaceous material.
❖ (basically it is formed in a combustion environment that is
‘oxygen starved’ and doesn’t form carbon dioxide
Sources of CO
❖ Incomplete combustion
❖ Automobile exhaust
❖ Fire
❖ Tobacco smoke (y’all gonna die)
❖ Endogenous CO — from heme degradation
Epidemiology

❖ 50,000 people a year seek help for CO poisoning


❖ 6,000/year of accidental deaths & 2000 suicides a year
due to CO poisoning
‣ 74% of the suicides were actually men
❖ Burning charcoal/fossil fuel is fast becoming the new
way of committing CO suicide
How CO enters & affects the body
❖ CO is usually inhaled — this is toxic to all organisms that depend on oxygen
❖ Poisoning may be:
❖ Acute — sudden onset
❖ Chronic — gradual onset
❖ Common symptoms include:
❖ Headache
❖ Nausea
❖ Seizures
❖ Tachycardia
❖ Loss of consciousness
❖ In severe cases, death
Pathophysiology of CO
1. Carbon monoxide is inhaled
2. In the lungs, gas exchange occurs. Normally oxygen is
exchanged for carbon dioxide, however when CO is
inhaled, haemoglobin has x230!!! times more affinity for
CO than for oxygen
3. Thus haemoglobin binds to CO forming
carboxyhemoglobin — this is very stable
4. As long as CO is attached to haemoglobin, oxygen cannot
be there too, thus this leads to hypoxia
❖ CO binds to cardiac myoglobin with an even greater affinity than to hemoglobin;
resulting in myocardial depression and hypotension exacerbates the tissue hypoxia

❖ CO can produce direct cellular changes involving immunological or inflammatory


damage by a variety of mechanisms, including the following : [2]

❖ Binding to intracellular proteins (myoglobin, cytochrome a,a )
 3

❖ Nitric oxide generation leading to peroxynitrite production


❖ Lipid peroxidation by neutrophils


❖ Mitochondrial oxidative stress


❖ Apoptosis


❖ Immune-mediated injury


❖ Delayed inflammation


❖ Following severe intoxication, patients display central nervous system (CNS) pathology,
including white matter demyelination. This leads to edema and focal areas of necrosis.
Acute poisoning
❖ Early — non-specific
❖ CNS & the heart is most
❖ 2 classical features (rare):
affected
❖ Cherry red colour —
blood & tissues ❖ Headache, nausea &
❖ Cutaneous bulla/blisters fatigue — mimics
influenza and food
❖ Based on severity:
poisoning
❖ Mild <30%
❖ Moderate 30-40%
❖ Tachycardia & change in
metal status occurs later
❖ Severe >40%
Chronic Poisoning
❖ May not follow the same symptoms as acute poisoning
❖ However long-term exposures may result in long-term
neuropsychiatric sequelae
❖ Mucous membranes of the body will almost never be
cherry pink.
❖ It is usually mistaken for chronic fatigue syndrome, as
patients usually present with polycythemia, increased
Ht etc.
Treatment
❖ Immediate removal from the contaminated area
❖ Goal of CO therapy is to improve oxygenation to the vital organs (heart &
brain)
❖ Hyperbaric oxygen is used, where the amount of oxygen is x30 greater than
normal.
❖ This shortens the half life of HbCO, reaching to 1hour (usually 4-6
hours)
Detectors
1. Opto-chemical — low cost detector; has a cloth pad that turns
dark in the presence of CO, no alarm device.
2. Biomemetic — has synthetic Hb which also darkens in the
presence of CO, both photoelectric light sensor & alarm
3. Electromechanical — produces electrical current relates to
CO, runs on minimum power but highly accurate
4. Semiconductor — produces an electrical current that precisely
relates to CO, highly accurate. Resistance to current in the
sensing element triggers alarm, but it uses a lot of power
Thank you

Ioana Cozma

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