Toxicity,
Carbon Monoxide
中山医院急诊科 姚晨玲
Background
? Carbon monoxide (CO) is a colorless,
odorless gas produced by incomplete
combustion of carbonaceous material
? CO is formed as a by-product of burning
organic compounds
Pathophysiology
? CO toxicity causes impaired oxygen
delivery and utilization
? CO reversibly binds hemoglobin,
resulting in relative anemia,
– CO binds hemoglobin 230-260 times more
avidly than oxygen,
– dissociation of CO from HbCO is slow than
that of O2 from HbO2 (1/3600)
Pathophysiology
? Resulting a leftward shift in the
oxyhemoglobin dissociation curve
? binds to cardiac myoglobin,resulting
myocardial depression and hypotension
? CO binds to cytochromes c and P450,
impaired oxygen utilization at the
cellular level,
Clinical
? Acute carbon monoxide poisoning
– Mild poisoning
? COHb level,10%-20%,
? Headache,nausea,vomiting,fatigue,
– Moderate poisoning
? COHb level,30%-40%,
? Confusion,Agitation,Hallucination,Visual disturbance,
syncope,seizure
? Skin,Classic cherry red skin is rare (ie,“When you're
cherry red,you're dead”); pallor is present more often,
– Severe poisoning
? COHb level,40%-60%,
? Noncardiogenic pulmonary edema,arrhythmia,
Papilledema
? delayed neuropsychiatric symptoms
– Long-term exposures or severe acute exposures
frequently result in long-term neuropsychiatric
sequelae,Additionally,some individuals develop
delayed neuropsychiatric symptoms,often after
severe intoxications associated with coma (about
3%-10% of all patients)
– After 2-60days,normal period”,chronic
headaches,memory problems,and parkinsonian-
type tremor,re-occur,
Clinical
delayed neuropsychiatric symptoms
[病例介绍 ] 年近半百的李某，湖南常宁市人，在新疆打工。
2002年 11月 27日晚，李某和另外 2人睡在生火炉的房内，次
日被人发现因煤气中毒昏迷，生命垂危。患者立即被送入
医院进行高压氧治疗 1次后，均神志清楚。李某于 11月 29日
自行乘火车返回湖南常宁，回家后生活尚能自理就未再进
行其他治疗。约 20天后，李某开始出现少气懒言、情感淡
漠、反应迟钝等症状，而且外出后不知道回家。家人以为
他中了“邪”，先后请巫婆念咒“安神”、“驱鬼”，患
者不仅不见好转，反而四肢瘫软，卧床不起，大小便失禁，
完全失语 …… 本月上旬，患者被送入湘雅医院，诊断为急
性一氧化碳中毒迟发性脑病。给予高压氧及细胞活化剂治
疗目前患者病情已有好转。
Lab Studies
? HbCO analysis
– Elevated levels are significant; however,
low levels do not rule out exposure,
especially if the patient already has
received 100% oxygen or if significant time
(8h) has elapsed since exposure
? Arterial blood gas
– PaO2 levels should remain normal,Oxygen
saturation is accurate only if directly
measured but not if calculated from PaO2,
which is common in many blood gas
analyzers,
– PCO2 levels is normal or mildly decreased
Lab Studies
? EEG
? CT scan
Lab Studies
Diagnosis
? History
? Clincal
? Lab studies
Differentials
? Toxicity,Sedative-Hypnotics
? Stroke
? Diabetic Ketoacidosis
? Neoplasms,Brain
Treatment
? Prehospital Care,
– Promptly remove from continued
exposure
? Emergency Department Care
– Continue 100% oxygen therapy until patient is
asymptomatic and HbCO levels are below 10%,
– Perform intubation for the comatose patient or,if
necessary,for airway protection
– Early blood samples may provide much more
accurate correlation between HbCO and clinical
status; however,do not delay oxygen
administration to acquire them,
– cardiac monitoring
Treatment
Treatment
? Hyperbaric oxygen therapy (HBO)
The rationale for the use of HBO
i) HBO produces a more rapid reduction in COHb levels,
The half-life of COHb is
4-5 hours in a person at rest breathing room air,
80 minutes by administration of 100% oxygen at sea level
22-23 minutes by treatment with hyperbaric oxygen (HBO) at 3
atmospheres absolute (ATA)
ii) HBO induces cerebral vasoconstriction,which may reduce intracranial
pressure and cerebral edema,
iii) HBO result in more rapid dissociation of CO from respiratory
cytochromes
iv) HBO may antagonize the oxidative injury that occurs after CO poisoning,
Treatment
? prevent and cure the cerebral edema
? recovery of cerebral function
Prognosis
prevent
Carbon Monoxide
中山医院急诊科 姚晨玲
Background
? Carbon monoxide (CO) is a colorless,
odorless gas produced by incomplete
combustion of carbonaceous material
? CO is formed as a by-product of burning
organic compounds
Pathophysiology
? CO toxicity causes impaired oxygen
delivery and utilization
? CO reversibly binds hemoglobin,
resulting in relative anemia,
– CO binds hemoglobin 230-260 times more
avidly than oxygen,
– dissociation of CO from HbCO is slow than
that of O2 from HbO2 (1/3600)
Pathophysiology
? Resulting a leftward shift in the
oxyhemoglobin dissociation curve
? binds to cardiac myoglobin,resulting
myocardial depression and hypotension
? CO binds to cytochromes c and P450,
impaired oxygen utilization at the
cellular level,
Clinical
? Acute carbon monoxide poisoning
– Mild poisoning
? COHb level,10%-20%,
? Headache,nausea,vomiting,fatigue,
– Moderate poisoning
? COHb level,30%-40%,
? Confusion,Agitation,Hallucination,Visual disturbance,
syncope,seizure
? Skin,Classic cherry red skin is rare (ie,“When you're
cherry red,you're dead”); pallor is present more often,
– Severe poisoning
? COHb level,40%-60%,
? Noncardiogenic pulmonary edema,arrhythmia,
Papilledema
? delayed neuropsychiatric symptoms
– Long-term exposures or severe acute exposures
frequently result in long-term neuropsychiatric
sequelae,Additionally,some individuals develop
delayed neuropsychiatric symptoms,often after
severe intoxications associated with coma (about
3%-10% of all patients)
– After 2-60days,normal period”,chronic
headaches,memory problems,and parkinsonian-
type tremor,re-occur,
Clinical
delayed neuropsychiatric symptoms
[病例介绍 ] 年近半百的李某，湖南常宁市人，在新疆打工。
2002年 11月 27日晚，李某和另外 2人睡在生火炉的房内，次
日被人发现因煤气中毒昏迷，生命垂危。患者立即被送入
医院进行高压氧治疗 1次后，均神志清楚。李某于 11月 29日
自行乘火车返回湖南常宁，回家后生活尚能自理就未再进
行其他治疗。约 20天后，李某开始出现少气懒言、情感淡
漠、反应迟钝等症状，而且外出后不知道回家。家人以为
他中了“邪”，先后请巫婆念咒“安神”、“驱鬼”，患
者不仅不见好转，反而四肢瘫软，卧床不起，大小便失禁，
完全失语 …… 本月上旬，患者被送入湘雅医院，诊断为急
性一氧化碳中毒迟发性脑病。给予高压氧及细胞活化剂治
疗目前患者病情已有好转。
Lab Studies
? HbCO analysis
– Elevated levels are significant; however,
low levels do not rule out exposure,
especially if the patient already has
received 100% oxygen or if significant time
(8h) has elapsed since exposure
? Arterial blood gas
– PaO2 levels should remain normal,Oxygen
saturation is accurate only if directly
measured but not if calculated from PaO2,
which is common in many blood gas
analyzers,
– PCO2 levels is normal or mildly decreased
Lab Studies
? EEG
? CT scan
Lab Studies
Diagnosis
? History
? Clincal
? Lab studies
Differentials
? Toxicity,Sedative-Hypnotics
? Stroke
? Diabetic Ketoacidosis
? Neoplasms,Brain
Treatment
? Prehospital Care,
– Promptly remove from continued
exposure
? Emergency Department Care
– Continue 100% oxygen therapy until patient is
asymptomatic and HbCO levels are below 10%,
– Perform intubation for the comatose patient or,if
necessary,for airway protection
– Early blood samples may provide much more
accurate correlation between HbCO and clinical
status; however,do not delay oxygen
administration to acquire them,
– cardiac monitoring
Treatment
Treatment
? Hyperbaric oxygen therapy (HBO)
The rationale for the use of HBO
i) HBO produces a more rapid reduction in COHb levels,
The half-life of COHb is
4-5 hours in a person at rest breathing room air,
80 minutes by administration of 100% oxygen at sea level
22-23 minutes by treatment with hyperbaric oxygen (HBO) at 3
atmospheres absolute (ATA)
ii) HBO induces cerebral vasoconstriction,which may reduce intracranial
pressure and cerebral edema,
iii) HBO result in more rapid dissociation of CO from respiratory
cytochromes
iv) HBO may antagonize the oxidative injury that occurs after CO poisoning,
Treatment
? prevent and cure the cerebral edema
? recovery of cerebral function
Prognosis
prevent
