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Carbon monoxide poisoning
Introduction 
• This deadly gas is one of the major causes of toxin-related 
deaths, amounting to at least 5000 deaths 
per year. Approximately 70% of these deaths are 
suicides. 
• CO is very common in the environment and usually 
arises from incomplete oxidation of reduced 
carbon. 
• An example is the automobile engine burning 
hydrocarbons. 
• Also, inadequate venting of devices that burn fossil 
fuels leads to the transfer of the gas to areas where 
people are sleeping, resulting in their deaths. 
• Cigarette smoke contains 5% CO. 
• Heaters 
• Fire fighters and fire victims
Pathophysiology 
CO has multiple toxic properties: 
• The major one is the displacement of O2 from 
hemoglobin, the O2 carrier protein, forming 
carboxyhemglobin (HbCO). Hemoglobin has a much 
stronger affinity for CO than it does for oxygen (200 
times). CO imparts a cherry pink discoloration to the 
skin (the inherent color of HBCO). 
• CO can also bind to myoglobin, another O2 carrier 
protein. Myoglobin (affinity is 40 times greater than 
oxygen) causing myocardial inhibition, hypotension 
(the degree of CNS toxicity depends on the degree of 
hypotension), ventricular arrhythmia, and cardiac 
arrest.
• CO has the capacity to inhibit cytochrome 
oxidase and cytochrome P450. 
All of these will diminish the overall level of 
oxidative respiration within the body.
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• CO has many effects on the heart. CO is 
known to cause gradual deterioration of 
myocardial function. It may produce 
ventricular arrhythmias and ECG 
abnormalities. When death occurs from CO, 
the immediate cause is believed to be 
myocardial ischemia (in case of high doses). 
• Neurological damages may occur.
Metabolism of CO 
• Pulmonary absorption depends on the duration of 
exposure, the concentration of CO in the 
environment and the alveolar ventilation rate. 
• 
• Approximately 1% of an inspired dose of CO is 
metabolized to CO2. 
• Pulmonary exhalation is the major pathway of CO 
elimination. 
• The half life of CO is about 4.5 hrs. The elimination 
of CO from the body depends greatly on the 
concentration of O2 because the 2 gases are 
competing for Hb. 80-90 min using oxygen therapy 
and 30 min using hyperbaric oxygen.
Signs and symptoms 
According to the measured carboxyhemoglobin level: 
• 10-20% Headache, dyspnea & weakness 
• 20-30% Severe headache & nausea may appear 
• 30-40% Severe headache, nausea & vomiting, ataxia, 
visual & auditory abnormalities & impaired judgment 
may be seen 
• 50-60% Confusion, syncope, seizures & coma 
Neurological complications: The degree of brain damage 
depends on the degree of hypoxia and hypotension. 
Headache is typically throbbing due to reflex 
vasodilation according to CNS hypoxia.
• CVS complications: Atrial and ventricular 
arrhythmia and ventricular fibrillation in severe 
cases. 
• Pulmonary complications: Shortness in breath 
and dyspnea, pulmonary edema and 
haemorrhage. 
• Kidney: Acute tubular necrosis and renal failure 
• Blood: Hemolytic anemia 
• Ophthalmic complications: Blurred vision and 
blindness 
• Skin: Pale or cyanosis skin
Chronic toxicity: 
- It is uncommon because CO does not 
accumulate. However, repeated exposure will 
cause accumulation of damage e.g. higher 
attitude, heavy smokers and pregnant 
woman. 
- The fetus is particularly vulnerable to CO 
poisoning. CO exposure leads to fetal death, 
anatomical malformation or decrease weight 
birth.
Treatment 
• Immediate removal from the contaminated 
area. 
• The goal of CO therapy is to improve 
oxygenation especially to the vital organs, 
the heart and brain. Hyperbaric O2 is used 
where; the amount of oxygen is 30 times 
greater than normal. Hyperbaric O2 shortens 
the half-life of the HbCO reaching 1 hr. 
•
• A blood sample for COHb assay should be 
obtained as early as possible and oxygen 
therapy continued while awaiting result. 
• In case of smoke inhalation, one must always 
alert for the possibility of toxicity from 
poisonous gases other than CO. 
• Hyperbaric oxygen has several disadvantages: 
- Most hospitals has no hyperbaric chamber, so 
the decision for patient traveling is important. It 
depends on severity of symptoms, patient's 
stability, and time for traveling. 
- Complications: emesis, seizures, agitation, & 
rupture of tympanic membrane.
Criteria for using hyperbaric oxygen: 
• Unconsciousness 
• Any acute or chronic neurological symptoms 
• Myocardial ischemia or arrhythmia 
• COHb > 40% 
• Pregnant woman with COHb > 8% 
• Metabolic acidosis with pH < 7.2
Carbon monoxide poisoning
Carbon monoxide poisoning
Carbon monoxide poisoning
Carbon monoxide poisoning

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Carbon monoxide poisoning

  • 2. Introduction • This deadly gas is one of the major causes of toxin-related deaths, amounting to at least 5000 deaths per year. Approximately 70% of these deaths are suicides. • CO is very common in the environment and usually arises from incomplete oxidation of reduced carbon. • An example is the automobile engine burning hydrocarbons. • Also, inadequate venting of devices that burn fossil fuels leads to the transfer of the gas to areas where people are sleeping, resulting in their deaths. • Cigarette smoke contains 5% CO. • Heaters • Fire fighters and fire victims
  • 3. Pathophysiology CO has multiple toxic properties: • The major one is the displacement of O2 from hemoglobin, the O2 carrier protein, forming carboxyhemglobin (HbCO). Hemoglobin has a much stronger affinity for CO than it does for oxygen (200 times). CO imparts a cherry pink discoloration to the skin (the inherent color of HBCO). • CO can also bind to myoglobin, another O2 carrier protein. Myoglobin (affinity is 40 times greater than oxygen) causing myocardial inhibition, hypotension (the degree of CNS toxicity depends on the degree of hypotension), ventricular arrhythmia, and cardiac arrest.
  • 4. • CO has the capacity to inhibit cytochrome oxidase and cytochrome P450. All of these will diminish the overall level of oxidative respiration within the body.
  • 6. • CO has many effects on the heart. CO is known to cause gradual deterioration of myocardial function. It may produce ventricular arrhythmias and ECG abnormalities. When death occurs from CO, the immediate cause is believed to be myocardial ischemia (in case of high doses). • Neurological damages may occur.
  • 7. Metabolism of CO • Pulmonary absorption depends on the duration of exposure, the concentration of CO in the environment and the alveolar ventilation rate. • • Approximately 1% of an inspired dose of CO is metabolized to CO2. • Pulmonary exhalation is the major pathway of CO elimination. • The half life of CO is about 4.5 hrs. The elimination of CO from the body depends greatly on the concentration of O2 because the 2 gases are competing for Hb. 80-90 min using oxygen therapy and 30 min using hyperbaric oxygen.
  • 8. Signs and symptoms According to the measured carboxyhemoglobin level: • 10-20% Headache, dyspnea & weakness • 20-30% Severe headache & nausea may appear • 30-40% Severe headache, nausea & vomiting, ataxia, visual & auditory abnormalities & impaired judgment may be seen • 50-60% Confusion, syncope, seizures & coma Neurological complications: The degree of brain damage depends on the degree of hypoxia and hypotension. Headache is typically throbbing due to reflex vasodilation according to CNS hypoxia.
  • 9. • CVS complications: Atrial and ventricular arrhythmia and ventricular fibrillation in severe cases. • Pulmonary complications: Shortness in breath and dyspnea, pulmonary edema and haemorrhage. • Kidney: Acute tubular necrosis and renal failure • Blood: Hemolytic anemia • Ophthalmic complications: Blurred vision and blindness • Skin: Pale or cyanosis skin
  • 10. Chronic toxicity: - It is uncommon because CO does not accumulate. However, repeated exposure will cause accumulation of damage e.g. higher attitude, heavy smokers and pregnant woman. - The fetus is particularly vulnerable to CO poisoning. CO exposure leads to fetal death, anatomical malformation or decrease weight birth.
  • 11. Treatment • Immediate removal from the contaminated area. • The goal of CO therapy is to improve oxygenation especially to the vital organs, the heart and brain. Hyperbaric O2 is used where; the amount of oxygen is 30 times greater than normal. Hyperbaric O2 shortens the half-life of the HbCO reaching 1 hr. •
  • 12.
  • 13. • A blood sample for COHb assay should be obtained as early as possible and oxygen therapy continued while awaiting result. • In case of smoke inhalation, one must always alert for the possibility of toxicity from poisonous gases other than CO. • Hyperbaric oxygen has several disadvantages: - Most hospitals has no hyperbaric chamber, so the decision for patient traveling is important. It depends on severity of symptoms, patient's stability, and time for traveling. - Complications: emesis, seizures, agitation, & rupture of tympanic membrane.
  • 14. Criteria for using hyperbaric oxygen: • Unconsciousness • Any acute or chronic neurological symptoms • Myocardial ischemia or arrhythmia • COHb > 40% • Pregnant woman with COHb > 8% • Metabolic acidosis with pH < 7.2