Carbon monoxide poisoning can occur from sources like space heaters, wood-burning stoves, and generators without adequate ventilation. CO binds to hemoglobin over 200 times more than oxygen, forming carboxyhemoglobin which impairs oxygen delivery. Clinical features include headache, confusion, vomiting, and loss of consciousness. Diagnosis is made through elevated carboxyhemoglobin levels and treatment involves high-flow supplemental oxygen and possibly hyperbaric oxygen therapy for more severe cases involving symptoms like syncope, seizures, or focal neurologic deficits.

1. Carbon Monoxide Poisoning
Sunil Kumar Daha
Janakpur, Nepal

2. • Potential Sources of Inhalation
• Space heaters
• Wood-burning stoves
• Charcoal burning for heat
• Portable generators without adequate ventilation
• Burn in a closed space
• Methylenechloride, found in varnishes and paint
strippers,

3. Pathophysiology
• CO is colorless, odorless gas
• Concentration in atmospheric air: 10ppm
• Toxicity begins at 100ppm
• Endogenously produced in the body during
normal breakdown of heme
• Normal physiologic
• Blood carbon monoxide levels from this
process are ~1% in healthy nonsmokers

4. Pathophysiology
• Binding affinity of normal adult hemoglobin
for carbon monoxide is about 200 times that
of oxygen
• Fetal hemoglobin has an even higher binding
affinity potentially more severe fetal toxicity
• Approximately 85% of carbon monoxide is
bound to hemoglobin and forms COHb
Rest is dissolved in plasma or bound intracellularly,
often to Myoglobin

5. Pathophysiology
Half-lives of COHb on room air at normal atmospheric
pressure: 249 -320 minutes
On 100% oxygen at atmospheric pressure: 74-80 minutes
COHb generated by methylenechloride exposure, which
can have a half-life of up to 13 hours due to ongoing
metabolism

6. Pathophysiology
•COHb does not provide oxygen delivery to the cells
•As COHb levels increase, relative anemia and hypoxia occurs
•Carbon monoxide shifts the oxyhemoglobin dissociation curve
to the left
Impaired oxygen release to the tissues

7. • Oxyhemoglobin(HbO2) dissociation curve

8. Cellular effects of CO
1.Lactic acidosis
CO inhibits intracellular cytochrome oxidase
interference with cellular respiration and ATP
generation relative uncoupling of oxidative
phosphorylation lactic acidosis
2.Endothelial dysfunction and vasodilatation
Due to release of Guanylatecyclase and nitric
oxide by CO
Leads to Hypotension

9. Cellular effects of CO
•The combination of relative hypoxia and hypotension can cause
ischemia-reperfusion injury in :
Cardiac myocytes
Neuronal tissue
•Results:
Rhabdomyolysis
Acute myocardial infarction
Neuronal cell death( mostly Cells in the basal ganglia involved, seen as
globuspallidus lesions in cranial CT

10. Clinical Features of acute CO toxicity
•History
Potential exposure to CO
Headache
Visual disturbances
Vomiting
Chest pain

11. Clinical Features contd..
•Physical Examination
Confusion
Ataxia
Dyspnea/tachypnea
Seizure
ECG changes/dysrhythmias
Syncope
Retinal hemorrhage
Bullousskin lesions
Focal neurologic deficit

12. • Diagnosis
• Elevated carboxyhemoglobinlevel
• Artificially elevated oxyhemoglobinsaturation using
pulse oximetry
• Elevated lactate
• Elevated anion gap metabolic acidosis
• Elevated creatinephosphokinase
• Elevated troponin
• Variable ECG findings—ranges from normal to injury
pattern(ST elevation MI)
• Bilateralglobuspalliduslesionson MRI

13. Caution!
•Standard pulse oximetry is unreliable in the diagnosis of CO
poisoning
•The wavelengths for COHbfall into the same range of those for
oxyhemoglobin,
which makes it difficult for standard pulse oximetry to differentiate
the two reading
•Thus pulse oximetry value of oxygen saturation will be higher than
the saturation on the ABG

14. Treatment
•Resuscitation ABCDE
•Supplemental oxygen in the highest concentrations
available should be initiated immediately
•Initiate hyperbaric oxygen (HBO) treatment as
required

15. Indications for Hyperbarric Oxygen
• Treatment of CO poisioning
• Syncope
• Confusion/altered mental status
• Seizure
• Coma
• Focal neurologic deficit
• Pregnancy with carboxyhemoglobinlevel
>15%
• Blood level >25%
• Evidence of acute myocardial ischemia

16. SYMPTOM SEVERITY DISPOSITION COMMENTS
Minimal or no symptoms Home Assess risk factors
Headache
Vomiting
Elevated CO level
Home after symptom
resolution
Administer 100% oxygen in
ED
•Observe 4 hrs
•Assess safety issues
Ataxia
Seizure
Syncope
Chest pain
Focal neurologic deficit
Dyspnea
ECG changes
Hospitalize
Consult with hyperbaric
specialist
Administer 100% oxygen in
ER
•Carbon monoxide level
Stability of the patient
must be considered for
transfer of hyperbaric
oxygen.

17. References
1. TintinallisEmergency Medicine A
Comprehensive Study Guide 7th Ed (2014)