Carbon monoxide poisoning can occur from incomplete combustion of carbon-containing materials like smoke or vehicle exhaust. CO binds to hemoglobin in blood over 200 times more than oxygen, reducing oxygen delivery to tissues. Symptoms range from headache and dizziness at low levels to organ damage, coma and death at high levels. Diagnosis involves exposure history and measuring carboxyhemoglobin levels. Treatment focuses on removing the patient from exposure and administering high-flow oxygen or hyperbaric oxygen to accelerate CO elimination from blood.
2. Introduction
• colorless, odorless, tasteless, and nonirritating
gas
• produced by the incomplete combustion of
any carbon-containing material
• Common sources - smoke inhalation in fires;
automobile exhaust fumes; faulty or poorly
ventilated charcoal, kerosene, or gas stoves;
and, to a lesser extent, cigarette smoke
3. Mechanism of toxicity
• consequence of cellular hypoxia and ischemia
– A. CO binds to hemoglobin with an affinity 250
times that of oxygen
• resulting in reduced oxyhemoglobin saturation and
decreased blood oxygen-carrying capacity
• oxyhemoglobin dissociation curve is displaced to the
left, impairing oxygen delivery at the tissues
4. – B. CO may also directly inhibit cytochrome
oxidase, further disrupting cellular function, and it
is known to bind to myoglobin, possibly
contributing to impaired myocardial contractility
– C. Postanoxic injury in the brain
• complicated by lipid peroxidation
• excessive release of excitatory neurotransmitters
• inflammatory changes
• adherence of neutrophils to cerebral vessels
5. – D. Fetal hemoglobin is more sensitive to binding
by CO
• fetal or neonatal levels may be higher than maternal
levels
7. E. Pharmacokinetics
• The carboxyhemoglobin complex
– gradually dissociates after removal from exposure
– Half-life
• 200 minutes in room air
• 74 minutes (24- 148 mins) during treatment with high-
flow oxygen (tight-fitting mask or endotracheal tube)
• 12-20 minutes during hyperbaric oxygen therapy
8. • II. Toxic dose. The recommended workplace limit (ACGIH
TLV-TWA) for carbon monoxide is 25 ppm as an 8-hour
time-weighted average. The level considered immediately
dangerous to life or health (IDLH) is 1200 ppm (0.12%).
However, the duration of exposure is very important.
Whereas exposure to 1000 ppm (0.1%) eventually will
result in 50% saturation of carboxyhemoglobin, it may take
several hours to reach that level. In 1895 Haldane
experimented on himself by breathing 2100 ppm CO for
over an hour, and it was only after 34 minutes, when his
level would have been approximately 25%, that he
described a throbbing headache. Brief exposure to much
higher levels may produce a more rapid rise in CO-Hgb.
9. III. Clinical presentation
• Symptoms of intoxication are predominantly
in the brain and heart
• Majority
– headache, dizziness, and nausea
– Patients with coronary disease may experience
angina or myocardial infarction
– With more severe exposures, impaired thinking,
syncope, coma, convulsions, cardiac arrhythmias,
hypotension, and death may occur
10. – Although blood carboxyhemoglobin levels may
not correlate reliably with the severity of
intoxication
• levels greater than 25% are considered significant
• levels greater than 40–50% usually are associated with
obvious intoxication
11. – Survivors of serious poisoning
• may suffer parkinsonism and a persistent vegetative
state to subtler personality and memory disorders
– Exposure during pregnancy
• may result in fetal demise
12. CO Levels with Related Signs and
Symptoms
>5% - mild headache
6-10% - mild headache, SOB with exertion
11-20% - moderate headache, SOB
21-30% - worsening headache, nausea,
dizziness, fatigue
31-40% - severe headache, vomiting, vertigo,
altered judgment
41-50% - confusion, syncope, tachycardia
51 – 60% - seizures, shock, apnea, coma
13. Signs and Symptoms CO Poisoning
Carboxyhemoglobin levels of <15 – 20%
Mild severity
Headache – mild to moderate
Shortness of breath
Nausea and vomiting
Dizziness
Blurred vision
15. Signs and Symptoms CO Poisoning
Carboxyhemoglobin levels of 41 - 59%
Severe
Dysrhythmias, palpitations
Hypotension
Cardiac ischemia
Confusion
Respiratory arrest
Pulmonary edema
Seizures
Coma
Cardiac arrest
16. Signs and Symptoms CO Poisoning
Carboxyhemoglobin levels of >60%
Fatal
Death
Cherry red skin is not listed as a sign
An unreliable finding
17. IV. Diagnosis
• history of exposure
• cherry-red skin coloration or bright red venous
blood is highly suggestive
• (Pulse oximetry - falsely normal readings
because it is unable to distinguish between
oxyhemoglobin and carboxyhemoglobin)
18. • A. Specific carboxyhemoglobin concentration
• B. Other useful laboratory studies -
electrolytes, glucose, BUN, creatinine, ECG,
and pregnancy tests
– Metabolic acidosis suggests more serious
poisoning
– With smoke inhalation, obtain the blood cyanide
level and methemoglobin concentration
19. V. Treatment
• A. Emergency and supportive measures
– 1. Maintain an open airway and assist ventilation
if necessary
– 2. Treat coma and seizures if they occur
– 3. Continuously monitor the ECG for several hours
after exposure
– 4. also consider cyanide poisoning and
methaemoglobinaemia
20. • B. Specific drugs and antidotes
– Administer oxygen in the highest possible
concentration (100%)
– Use a tight-fitting mask and high-flow oxygen with
a reservoir (non rebreather) or administer the
oxygen by endotracheal tube
– Treat until the carboxyhemoglobin level is less
than 5%
– Consider hyperbaric oxygen in severe cases
21. • C. Decontamination
– Remove the patient immediately from exposure
and give supplemental oxygen
– Rescuers exposed to potentially high
concentrations of CO should wear self-contained
breathing apparatus
22. • D. Enhanced elimination
– Hyperbaric oxygen provides 100% oxygen and can
enhance elimination
– It remains unclear whether its benefits over
normobaric oxygen
23. • Proposed Indications for Hyperbaric Oxygen
– Age > 50 years
– Cerebellar dysfunction
– Loss of consciousness
– Metabolic acidosis
– CO Hgb > 25%