Carbon Monoxide Poisoning: Overview and Practice Questions

Carbon monoxide (CO) poisoning is a life-threatening condition caused by inhalation of CO gas, an odorless, colorless, and non-irritating substance.

Resulting from incomplete combustion of carbon-containing materials, this insidious toxin interferes with the body’s ability to transport oxygen, leading to cellular injury and death.

Given its invisibility and the nonspecific nature of its early symptoms, timely diagnosis and intervention are crucial to prevent severe morbidity and mortality.

What is Carbon Monoxide Poisoning?

Carbon monoxide poisoning occurs when one inhales excessive amounts of carbon monoxide (CO), an odorless, colorless gas. Produced by incomplete combustion of carbon-containing materials, CO interferes with the blood’s ability to carry oxygen, leading to potentially fatal health effects.

Symptoms

Carbon monoxide poisoning can manifest through a variety of symptoms. The severity often correlates with the concentration of CO inhaled and the duration of exposure.

Some common symptoms include:

• Headache
• Dizziness
• Weakness
• Upset stomach
• Vomiting
• Chest pain
• Confusion
• Blurred vision
• Shortness of breath
• Loss of consciousness

Note: The symptoms can be subtle and misleading, sometimes resembling other conditions like the flu. Immediate medical attention is vital if one suspects carbon monoxide poisoning.

Treatment

Carbon monoxide poisoning demands prompt intervention, with oxygen therapy using the highest available FiO2. Initially, 100% oxygen should be delivered via a nonrebreathing mask.

The pinnacle of therapeutic intervention is hyperbaric oxygen therapy, which immerses the patient in 100% oxygen at pressures exceeding that of sea level.

This procedure swiftly counters the effects of carbon monoxide poisoning by saturating tissues and organs with oxygen.

While hyperbaric oxygen therapy stands as the gold standard, its accessibility can be limited. In its absence, intubation and mechanical ventilation with an FiO2 of 100% may be necessary.

Blood Analysis for Carbon Monoxide Poisoning

When suspecting carbon monoxide poisoning, it’s imperative to analyze the patient’s blood sample using a CO-oximeter rather than a standard blood gas machine.

Relying on a standard blood gas analyzer can produce misleading carbon monoxide levels.

For instance, a patient with 50% carboxyhemoglobin might register an arterial oxygen saturation of 95% on a conventional blood gas machine, when, in reality, their actual oxygen saturation is a perilous 45%.

A CO-oximeter provides an accurate measurement of carbon monoxide levels in the blood, ensuring correct diagnosis and treatment for the patient.

Carbon Monoxide Poisoning Practice Questions

1. What is carbon monoxide?
Carbon monoxide is a colorless, odorless, nonirritating gas produced by the incomplete combustion of any carbon-containing material. It is harmful and can be very dangerous if a person inhales too much of this gas.

2. What is an abbreviation for carbon monoxide?
CO

3. As a respiratory therapist, when patients are suspected of carbon monoxide poisoning, what is the first thing that must be done to treat this patient?
Give them 100% oxygen as soon as possible.

4. What are common sources of CO?
Smoke inhalation from fires, automobile exhaust fumes, faulty/poorly ventilated charcoal, kerosene or gas stoves, and the temporary use of electrical generators.

5. What is the most effective method of treating carbon monoxide poisoning?
Place the patient in a hyperbaric oxygen chamber.

6. What does CO do in the body?
Binds to heme iron in hemoglobin with an affinity 250x that of O2, creating carboxyhemoglobin (CO-Hb) and causing tissue hypoxia.

7. What are the mechanisms of CO-induced hypoxia?
The presence of CO-Hb reduces oxyhemoglobin saturation and decreases blood O2-carrying capacity. CO-Hb shifts the oxyhemoglobin dissociation curve to the left, thereby impairing the dissociation of O2 from hemoglobin and impairing O2 delivery to the tissues.

8. How many oxygen binding sites are there for hemoglobin?
4

9. What does a left or right shift on the oxyhemoglobin curve represent?
Left shift: increased Hb-O2 affinity (O2 stays bound to Hb and cannot diffuse into the tissues). Right shift: decreased Hb-O2 affinity (O2 has trouble staying bound to Hb and prefers to be in the tissues).

10. Why does the oxyhemoglobin dissociation curve not form a straight line?
The binding of each oxygen molecule makes it easier for the next to bind (affinity increases with each oxygen molecule bound), so the curve has to be curved, and it shifts in either direction.

11. How does the presence of CO-Hb affect oxyhemoglobin saturation?
CO-Hb reduces oxyhemoglobin saturation and therefore reduces blood O2 carrying capacity.

12. How does the binding of CO at one of the oxygen sites affect oxygen’s affinity for the remaining three sites?
Oxygen’s affinity for the remaining three sites is dramatically increased, causing the O2 to stay bound and preventing it from diffusing into the tissues. This is similar to how when the 1st O2 binds to the site, it makes it easier for other O2 molecules to bind. The difference is that when it is only O2 binding, the affinity is not strong enough to prevent O2 from diffusing to hypoxic tissue.

13. What mechanism of CO poisoning can cause lactic acidosis?
CO binds to cytochrome c oxidase in the mitochondria, impairing oxidative phosphorylation and causing the body to switch to anaerobic metabolism. This results in lactic acidosis.

14. What mechanism of CO poisoning can cause reduced cardiac output and hypotension?
CO binds to myoglobin in the heart and skeletal muscle.

15. How does the CO-Hb complex dissociate after the removal from exposure?
Slowly

16. How can the CO-Hb T1/2 be significantly decreased?
Administration of O2 under pressure

17. What are the initial symptoms of CO poisoning?
Nonspecific symptoms include HA, fatigue, sleepiness, dizziness, sweating, N/V, confusion, and memory problems.

18. What patients could also experience angina or a myocardial infarction due to CO poisoning?
Patients with coronary disease

19. What are the severe symptoms of CO poisoning?
Impaired thinking, loss of consciousness, coma, convulsions, hypotension, cardiac arrhythmias, and death.

20. What is a sign of CO poisoning that can be seen on an autopsy but not in living victims?
Cherry red skin color

21. What two factors of CO exposure determine the patient’s toxicity?
The concentration of CO and duration of exposure.

22. What are the challenges of diagnosing a patient with CO poisoning?
The only easy CO poisoning diagnosis is when the patient has a known history of CO poisoning. Otherwise, there are no specific clinical findings, and conventional pulse oximetry gives falsely normal readings.

23. What tests can help diagnose carbon monoxide poisoning?
Blood CO-Hb concentration, EKG, blood electrolytes, and glucose.

24. What does it mean if a patient has both CO poisoning and metabolic acidosis?
More serious poisoning.

25. How is CO poisoning treated?
Decontamination (removal of the patient from the exposure); maintain an open airway and assist ventilation if necessary; oxygen (high-flow 100% O2, tight-fitting mask); hyperbaric O2 to speed up CO elimination if CO levels are above a certain threshold; treatment of seizures if they occur; and EKG monitoring.

26. What are some long-term consequences of CO poisoning?
At higher risk of developing neuropsychiatric sequelae such as persistent vegetative state, Parkinsonism, impaired concentration and memory, or mood disorders.

27. What is the mechanism of long-term consequences of CO poisoning?
Lipid peroxidation of neuronal cell membranes.

28. What is carboxyhemoglobin?
Hemoglobin bound to carbon monoxide, which is formed in the blood when carbon monoxide is inhaled, reducing the ability of the blood to form oxyhemoglobin.

29. What should be used to analyze the patient’s blood sample if carbon monoxide poisoning is suspected?
CO-oximeter

30. What are the symptoms of carbon monoxide poisoning?
Mild-moderate: headache, nausea, dizziness, poor feeding; severe: seizures, syncope, coma; can present with myocardial ischemia or arrhythmias; and delayed neuropsychiatric syndrome.

31. What are the signs of carbon monoxide poisoning?
Mental state changes are the most common physical finding and the “cherry red” appearance of the lips and skin.

32. What is neuropsychiatric syndrome in CO poisoning?
Occurs in up to 40% of cases within 20 days of significant exposure; features include cognitive deficit, behavior change, and focal neurological deficits. Symptoms may persist for one year. Cannot predict likelihood based on initial carboxyhemoglobin levels. Often associated with loss of consciousness at the time of intoxication.

33. What is the diagnosis of carbon monoxide poisoning?
Exposure and elevated carboxyhemoglobin levels; pulse oximetry cannot distinguish between oxyhemoglobin and carboxyhemoglobin.

34. At what COHb % will someone die from CO poisoning?
60%

35. What is methemoglobin?
Hemoglobin that cannot bind to O2 due to oxidation of Fe2+ to Fe3+. The remainder of the heme molecules will have an increased affinity for O2 (i.e., left shift).

36. What are the common sources of carbon monoxide?
The product of incomplete (internal) combustion of hydrocarbons (engine exhaust), fire, improperly adjusted heating elements, charcoal/gas grills, exposure to paint strippers containing methylene chloride, and tobacco smoke.

37. What oxygen Hb dissociation curve changes occur with carbon monoxide poisoning?
Because of its high affinity for Hgb, there is a left shift, resulting in impaired O2 release at the tissue level with resultant cellular hypoxia.

38. What are some more clinical signs and symptoms of carbon monoxide poisoning?
Headache, nausea, vomiting, syncope, seizures, angina, pulmonary edema, arrhythmias, and fetal distress if pregnant.

39. What are the important factors of the carboxyhemoglobin levels of persons who die from CO poisoning?
Source of the CO, circumstances surrounding the death, and the individual’s health.

40. Why do CO poisoning deaths sometimes have skin slippage?
CO diverted into a vehicle or other small area can significantly raise the temperature of this space, which can account for postmortem skin slippage in some cases.

41. What kind of shift to the oxyhemoglobin dissociation curve does CO poisoning cause?
Left shift

42. What is the most common cause of CO poisoning resulting in death?
Fires

43. What is the second common cause of CO poisoning resulting in death?
Inhalation of vehicle exhaust fumes; most of these deaths are suicides.

44. What percentage of carboxyhemoglobin level (CO-HB) is concerning in non-pregnant patients?
Greater than 25%

45. What percentage of carboxyhemoglobin level (CO-HB) is concerning in pregnant patients?
Greater than 10%

46. What is the second common cause of CO poisoning resulting in death?
Inhalation of vehicle exhaust fumes; most of these deaths are suicides.

47. What is the most common cause of CO poisoning resulting in death?
Fires

48. What are the physical findings of carboxyhemoglobinemia?
Carbonaceous sputum, facial burns, singed nasal hairs, signs of hypoxemia, rapid respiratory rate, nasal flaring or intercostal retractions, hoarse voice, grunting, rales or rhonchi, erythema or edema of oropharynx or nasopharynx, and the inability to swallow.

49. What are the four signs of hypoxemia?
Agitation, anxiety, stupor, and cyanosis.

50. What diagnostic tests are not useful for CO poisoning?
Routine ABG and pulse oximetry.

51. What is the diagnosis of carbon monoxide poisoning?
Arterial or venous carboxyhemoglobin saturation.

52. What are the indications for treating CO-poisoning patients with hyperbaric oxygen?
History of loss of consciousness, carboxyhemoglobin greater than 25%, metabolic acidosis, age greater than 50, and cerebellar findings on a neurologic exam.

53. Does carbon monoxide poisoning occur at a specific time of year?
No, it can happen at any time.

54. What are the physical properties of carbon monoxide?
It’s a colorless, odorless, tasteless, non-irritating gas.

55. What are the most common sources of CO in deaths?
Fires, automobile exhaust, defective heaters, and incomplete combustion of burning products.

56. When is CO produced?
Whenever organic materials are burned with an inadequate oxygen supply necessary to produce complete combustion.

57. What are the sources of CO in the home?
Furnace, charcoal grill, range, water heater, automobile in a closed garage, fireplace, gas, and clothes dryer, etc.

58. How many deaths are caused by CO in the U.S. annually?
Approximately 2,700 deaths (excluding fire deaths).

59. How many deaths caused by CO in the U.S. per year are due to suicide?
Approximately 2,000 deaths

60. How many deaths caused by CO in the U.S. per year are due to accidents?
Approximately 700 deaths

61. Are deaths due to CO more commonly because of suicide or accidents?
Suicide is more likely the cause.

62. What is the most common suicide due to CO poisoning?
The inhalation of automobile exhaust

63. What are the mechanisms of action in CO poisoning?
CO produces tissue hypoxia by competing with oxygen for binding sites on the oxygen-carrying hemeproteins (hemoglobin, myoglobin, etc.). Carbon monoxide displaces oxygen atoms, while hemoglobin is full of carbon monoxide and cannot deliver oxygen to the cells.

64. What molecule does CO compete with oxygen for binding?
Hemeproteins (i.e., hemoglobin and myoglobin)

65. What has a greater affinity for hemoglobin between CO and oxygen?
CO

66. How much greater is the affinity of CO for hemeproteins compared to oxygen?
30 to 500 times greater

67. How much greater is the affinity of CO for hemoglobin compared to oxygen?
250 to 300 times greater

68. Why is carbon monoxide toxic?
It is believed that CO has toxic effects at the cellular level by impairing mitochondrial respiration.

69. Is a lot of CO in the atmosphere required in order to produce high carboxyhemoglobin levels?
No, there only needs to be a little.

70. What is the “normal” level of carboxyhemoglobin for smokers?
The normal level is 5-6%, but it commonly reaches 10% and can even exceed 15%.

71. Is a smoker more likely to have more CO in their body than a nonsmoker?
Yes

72. What are the symptoms at 10% COHb?
No symptoms; heavy smokers can have as much as 10 to 15% COHb.

73. What are the symptoms at 15% COHb?
Mild headache

74. What are the symptoms at 25% COHb?
Nausea and a serious headache; fairly quick recovery after treatment with oxygen and/or fresh air.

75. What are the symptoms at 30% COHb?
Symptoms intensify; potential for long-term effects, especially in the case of infants, children, the elderly, victims of heart disease, and pregnant women.

76. What are the symptoms at 40 to 60% COHb?
Mental confusion, weakness, loss of coordination, and unconsciousness.

77. What are the symptoms at 60%+ COHb?
Death

78. How long does it take to show signs of carbon monoxide poisoning?
Symptoms can appear within minutes to hours, depending on the concentration and duration of exposure.

79. What can carbon monoxide poisoning be mistaken for?
It can be mistaken for the flu, food poisoning, or other viral infections due to similar symptoms.

80. How quickly does carbon monoxide make you sick?
Exposure to high levels can make you sick within minutes.

Final Thoughts

 

Carbon monoxide poisoning remains a critical medical emergency that requires prompt recognition and intervention.

As healthcare professionals, understanding the subtleties of its presentation and the nuances in treatment is vitally important.

Though the symptoms can mimic other ailments, swift and accurate diagnosis, followed by the appropriate therapeutic measures, can mean the difference between life and death.

As with many health hazards, prevention and education are the primary tools in the fight against this silent threat.