Download carbon monoxide poisoning

CARBON MONOXIDE
POISONING
DANA BARTLETT, BSN, MSN, MA, CSPI
Dana Bartlett is a professional nurse and
author. His clinical experience includes 16
years of ICU and ER experience and over 20
years of as a poison control center information
specialist. Dana has published numerous CE
and journal articles, written NCLEX material,
written textbook chapters, and done editing
and reviewing for publishers such as Elsevire,
Lippincott, and Thieme. He has written widely
on the subject of toxicology and was recently
named a contributing editor, toxicology section, for Critical Care Nurse journal. He is
currently employed at the Connecticut Poison Control Center and is actively involved
in lecturing and mentoring nurses, emergency medical residents and pharmacy
students.
ABSTRACT
Known as the silent killer, carbon monoxide poisoning in individuals
can present in various ways and the medical literature continues to
contain areas of uncertainty and controversy. Symptoms of carbon
monoxide poisoning tend to be non-specific in mild and severe cases.
Delayed neuropsychiatric effects can occur, which are considered a
serious complication. Diagnosis of carbon monoxide poisoning is based
upon the patient history and physical examination as well as an
elevated carboxyhemoglobin level. The etiology, clinical presentation
and treatment are discussed, including those for children and special
cases such as pregnancy.
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Policy Statement
This activity has been planned and implemented in accordance with
the policies of NurseCe4Less.com and the continuing nursing education
requirements of the American Nurses Credentialing Center's
Commission on Accreditation for registered nurses. It is the policy of
NurseCe4Less.com to ensure objectivity, transparency, and best
practice in clinical education for all continuing nursing education (CNE)
activities.
Continuing Education Credit Designation
This educational activity is credited for 2 hours. Nurses may only claim
credit commensurate with the credit awarded for completion of this
course activity.
Statement of Learning Need
Carbon monoxide poisoning is a common and potentially fatal event
with nonspecific clinical findings. Clinicians knowledgeable in the
identification and treatment of carbon monoxide poisoning can help to
initiate neuroprotective interventions and improve patient outcomes.
Course Purpose
This course will help clinicians identify carbon monoxide (CO)
exposures and the standard treatments for CO poisoning.
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Target Audience
Advanced Practice Registered Nurses and Registered Nurses
(Interdisciplinary Health Team Members, including Vocational Nurses
and Medical Assistants may obtain a Certificate of Completion)
Course Author & Planning Team Conflict of Interest Disclosures
Dana Bartlett, RN, MA, MSN, CSPI, William S. Cook, PhD,
Douglas Lawrence, MA, Susan DePasquale, MSN, FPMHNP-BC – all
have no disclosures
Acknowledgement of Commercial Support
There is no commercial support for this course.
Please take time to complete a self-assessment of knowledge,
on page 4, sample questions before reading the article.
Opportunity to complete a self-assessment of knowledge
learned will be provided at the end of the course.
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1.
Carbon monoxide is produced by:
a. incomplete combustion of carbon-containing fuel
b. combustion of nitrogen-containing materials
c. vapors emitted from carbon-containing fuel
d. combustion of in organic acids
2.
Carbon monoxide can also be produced by:
a. toluene
b. methylene chloride
c. cyanide
d. cadmium
3.
One of the basic ways by which CO causes harm is:
a. decreased production of hemoglobin
b. production of abnormal hemoglobin
c. tissue hypoxia
d. pulmonary and coronary vasoconstriction
4.
One of the basic ways by which CO causes harm is:
a. damage to pulmonary capillaries
b. production of methemoglobin
c. hemolysis
d. direct cellular toxicity
5.
Two organs particularly vulnerable to CO poisoning are:
a. the brain and the heart
b. the kidneys and the pancreas
c. the thyroid gland and the small bowel
d. the lungs and the liver
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Introduction
Carbon monoxide (CO) is sometimes called the silent killer, and aptly
so. It is a gas that is produced by incomplete combustion of carboncontaining material, it is colorless, odorless, and tasteless, and CO can
be lethal. Despite large-scale public education and prevention
programs, CO exposure is still a serious public health problem. The
pathophysiology, clinical effects, and the best methods for treating CO
poisoning have been intensively studied, but there are still areas of
uncertainty and controversy.
Epidemiology
As mentioned in the introduction, despite increased public awareness
of the dangers of CO and widespread public education and prevention
measures, CO poisoning is still very common. Many sources consider
CO poisoning to be among the leading causes of poisoning deaths in
the United States, and CO poisoning is perhaps the number one
worldwide cause of death by poisoning.1,2,3
Carbon monoxide is produced by the incomplete combustion of
carbon-containing material. Automobile exhaust and home heating
and/or cooking systems that use oil, gas, coal, or wood are the most
common causes of CO poisoning, excluding exposures to fires. Carbon
monoxide is also produced when tobacco is burned.
Exposures to carbon monoxide and cases of CO poisoning can happen
at any time of the year but are more common during the winter
months. If temperatures are particularly cold and/or there is a power
outage, people may attempt to heat their homes in ways that are
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unsafe. In 2011, in Connecticut, a heavy snowstorm caused a
widespread power outage and ambient temperatures at the time were
quite cold. Emergency rooms in the state were inundated with cases of
carbon monoxide poisoning as people were using gasoline generators
and charcoal burning grills inside their homes to try and stay warm.4
Two other sources of carbon monoxide are methylene chloride and
methylene iodide. Methylene chloride is a chemical that is often used
as a component of commercially available paint strippers. Inhaled
methylene chloride vapors or methylene chloride that is ingested or
dermally absorbed is converted in vivo to CO. Because it is stored in
fat tissues and the metabolizing enzymes are quickly saturated, peak
CO levels produced by methylene chloride inhalation, ingestion, or
dermal absorption are seen 8 hours or longer after an exposure.5
Methylene iodide is used by jewelers to examine gems and, like
methylene chloride, it is converted in vivo to CO.6 Carbon monoxide
poisoning caused by either of these is very uncommon.
Carbon Monoxide: Pathophysiology
The traditional and commonly understood mechanism of CO poisoning
is that CO preferentially binds to hemoglobin, displacing oxygen from
hemoglobin binding sites and causing cellular and tissue hypoxia. The
binding of CO to hemoglobin and the reduced oxygen delivery to
tissues and organs is certainly one of the primary ways that CO acts a
poison. But research has shown that CO poisoning is much more
complex and there are multiple, dynamic processes by which CO
causes harm.
7-13
Some of these are known to affect humans and
some have only been found in animal models.
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Hemoglobin Binding
Carbon monoxide binds avidly to hemoglobin: it has an affinity for
hemoglobin that is 200-250 times greater than that of oxygen. When
CO displaces oxygen from hemoglobin and CO occupies the binding
sites for oxygen on hemoglobin, this results in CO and hemoglobin
combining to form carboxyhemoglobin (COHb). Carboxyhemoglobin
does not bind with oxygen, so most of the hemoglobin is rendered
functionally useless.
Oxygen Transfer and the Oxyhemoglobin Dissociation Curve
The oxyhemoglobin dissociation indicates how saturated hemoglobin is
at any particular level of oxygen tension of the blood. It also indicates
how tightly hemoglobin holds on to oxygen and how easily it releases
oxygen for transfer to the tissues. Carbon monoxide shifts the
oxyhemoglobin dissociation curve to the left so for any particular level
of oxygen saturation less oxygen will be transferred to the tissues.
This happens for two reasons. First, CO greatly increases the
attachment of oxygen to hemoglobin. Second, because there is very
little oxygen bound to hemoglobin, the difference between the oxygen
level in tissues and the oxygen level of hemoglobin is greatly
decreased.
This difference is usually a strong driving force for the transfer of
oxygen from hemoglobin to the tissues, but it is significantly
diminished by the presence of CO. In CO poisoning the oxyhemoglobin
dissociation curve shifts to the left and less oxygen reaches the
tissues.
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Binding to Myoglobin
Myoglobin is an oxygen-transporting and storage pigment that is found
inside cells. Carbon monoxide binds to myoglobin - particularly in the
myocardium - thus preventing oxygen utilization.
Interference with Oxidative Phosphorylation
Carbon monoxide binds with mitochondrial cytochrome oxidase, an
important enzyme that is needed for proper functioning of the electron
transport chain in cellular respiration that produces the bulk of the
adenosine triphosphate (ATP) needed by the body.
Vasodilation
Carbon monoxide increases the formation of cyclic guanosine
monophosphate. Cyclic guanosine is second messenger similar to
cyclic adenosine monophoshosphate cAMP). Second messengers act to
transfer the effects of hormones and other compounds that cannot
pass through cell membranes. Cyclic guanosine causes the release of
nitric acid from platelets and the vascular endothelium. Cyclic
guanosine monophosphate and nitric oxide are potent vasodilators,
blood is pooled in the vascular bed, and this decreases oxygen delivery
to the tissues.
Free Radical Formation
High levels of nitric oxide initiate the formation of free radicals, and
the tissue damage that is caused by poor perfusion stimulates an
inflammatory response and free radical formation. The result is a
reperfusion injury that can affect the brain and other parts of the
central nervous system.
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Lipid Peroxidation
Carbon monoxide poisoning causes lipid peroxidation. Lipid
peroxidation refers to damage caused by free radicals to the lipids that
are an integral part of cell membranes. This process is thought to be
one of the causes of the neurological effects of CO poisoning.
Leukocyte-Mediated Inflammation
There is evidence that the oxidative stress induced by free radicals
causes neutrophils to adhere to cerebral microvasculature. The result
is an inflammatory process that may be the cause of the acute and
delayed neurological damage that is a common feature of CO
poisoning.
Apoptosis
Apoptosis is the process of programmed cell death. Carbon monoxide
poisoning is thought to accelerate the process of apoptosis.
Cardiac Stunning
Carbon monoxide is thought to at times produce a catecholamine
surge and this can cause what is called myocardial stunning - a
temporary, non-ischemic ventricular dysfunction.
Thrombus Formation
Carbon monoxide can inhibit or impair fibrinolysis and increase the
amount of thrombin that is formed. Thromboembolic complications
caused by CO poisoning have been reported.
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The contribution of each of these to CO poisoning is not clearly
understood. Carbon monoxide clearly causes tissue hypoxia and
decreased oxygen utilization at the cellular level. Those mechanisms
are probably responsible for the immediate signs and symptoms of CO
poisoning that are so familiar to and recognized by health care
personnel.
Carboxyhemoglobin levels that reflect tissue hypoxia do not always
correlate with the severity of signs and symptoms.14,15 Patients do not
always improve as CO is eliminated, and animal experiments have
shown that transfused blood with a high level of CO will cause a very
high COHb level, but this is less toxic than lower levels of CO that are
inhaled.16 Carbon monoxide poisoning then, is probably caused by
tissue hypoxia and by direct cellular poisoning. How, why, and when
these processes affect a patient who has been exposed to CO is not
known.
The mechanisms by which CO poisoning produces signs and symptoms
are complex and still not completely understood. Research is ongoing
and there are probably other ways that CO causes harm. However, the
basic effects of CO poisoning are a) decreased oxygen delivery, b)
decreased oxygen utilization, and c) direct toxic injuries to the tissues.
The Endogenous Production Of Carbon Monoxide
Carbon monoxide is an endogenous compound produced by the
breakdown of hemoglobin, lipid peroxidation, and the metabolism of
xenobiotics (substances foreign to the body). The normal level of
COHb is approximately 0.1-1%. In the past several decades, many
functional roles of CO have been identified. Carbon monoxide acts as a
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neural messenger and a vasodilator, it inhibits platelet aggregation,
and it appears also to protect against apoptosis, cell proliferation,
inflammation, and vasoconstriction.17-19 In vitro and animal studies
have shown that CO could be used therapeutically, possibly as a
potent anti-inflammatory to treat ischemia-reperfusion injury, lung
injury, sepsis, or pathological processes, such as multiple sclerosis,
that are characterized by inflammation.
Caring For A Patient With CO Poisoning
Are you a clinician caring for a patient who has CO poisoning? That
may seem like an odd question because the situation and the patient’s
complaints quite often make it obvious that a CO exposure has
occurred. The patient states that her/his home heating system
malfunctioned, the CO detector was alarming, and the patient has
common signs and symptoms of CO poisoning.
Remember, CO is called the silent killer. It is colorless, odorless and
tasteless, and some exposures to CO can be easily overlooked. Occult
CO exposures, poisonings in which CO was not initially identified as the
cause of the patient’s complaints, which prompt a patient to seek
medical attention, are relatively common; and, CO poisoning
frequently produces a clinical picture that is vague and non-specific.
Carbon monoxide poisoning can be mistaken for drug overdose,
encephalitis, hypoglycemia, influenza, migraine headache, or other
pathologies. Aside from knowing the common signs and symptoms of
CO poisoning, the health team must also know and be able to
recognize the circumstances and situations that are likely to cause
exposure to CO.
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If CO poisoning is suspected and the attending health team wants to
determine if CO poisoning has occurred, the patient(s) and/or their
significant other needs to be asked the following questions.

Where were you when you began to feel sick? If you were at
home was the heating system on? If these signs and symptoms
have occurred before, do they only happen when you are at
home? Do they improve when you are out of the house? Does
the patient have a functioning CO detector?

Who do you live with? Has anyone else been sick? If yes, what
are their symptoms? If the patient is living with other people but
no one else is sick, CO exposure is unlikely.

Has your heating system, water heater, etc., and the exhaust
systems and chimneys in your house been checked recently?

Do you get sick when you are driving your car? Do your
symptoms improve after you leave the car? Has your car’s
exhaust system been inspected recently?

Do the symptoms happen while you are at work? If so, what
does the patient do, and what is happening at work when he/she
gets sick? Does the patient work inside? If yes, are there obvious
sources of CO? Is the patient a mechanic working in a poorly
ventilated garage, or is he/she working in a building where gaspowered or gasoline-powered machinery is operating?

Has the patient been stripping furniture?
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
If there is more than one patient and everyone has essentially
the same signs and symptoms, determine if all of the patients
got sick at the same time (indicating possible CO poisoning) or
did the illness start with one person and seem to spread to the
others (indicating a possible infectious illness).
Signs And Symptoms Of Carbon Monoxide Poisoning
Carbon monoxide poisoning can be
difficult to detect because the
symptoms may be mild and even in
severe cases they are non-specific.
Also, the number and intensity of the
If there is no obvious or
known exposure to CO, a mild
CO exposure can be
overlooked or misdiagnosed.
signs and symptoms of CO poisoning
is not always related to the COHB level (discussed in more detail later
on the learning module).14,15,20 Patients with low levels may be sicker
than patients with high levels.
Because CO impairs oxygen delivery and utilization, organs that are
very metabolically active, such as the brain and the heart, are most
affected by CO. The heart and the brain are also susceptible to direct
cellular poisoning as CO has toxic mechanisms that affect those
organs. The elderly, children (possibly), people with anemia,
cardiovascular disease, or pulmonary disease, and people who smoke
have a higher risk of developing CO poisoning than do healthy
individuals or those who are neither very young nor very old. The
severity of CO poisoning depends on patient risk factors and on the
particulars of the exposure: the higher the CO level and the longer the
time of exposure, the sicker the patient is likely to be.
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CO Symptom Severity
The clinical picture of CO poisoning can be divided into mild, moderate,
and severe. Patients with mild CO will have confusion, dizziness,
fatigue, headache, nausea, and tachycardia. Patients with moderate
CO poisoning will have ataxia, chest pain, dyspnea, syncope, and
tachycardia. Patients with severe CO poisoning will have arrhythmias,
coma, hypotension, metabolic acidosis, and seizures. There can be
considerable overlap in the signs and symptoms of the presentation,
and it is helpful to think of CO poisoning as a continuum of signs and
symptoms, caused by tissue hypoxia and direct cellular toxicity that
affect vulnerable organs.
As mentioned previously, the heart is particularly vulnerable to
damage from CO because it is so metabolically active and has a very
high need for oxygen. The heart is also affected by mechanisms of
injury that cause direct cellular damage. Cardiovascular signs and
symptoms, from mild to serious, are very common after CO exposure.
Patients often have palpitations and tachycardia and may develop
angina, arrhythmias, cardiogenic shock, cardiomyopathy, heart failure,
non-specific ST segment and T wave changes, pulmonary edema, and
ST-segment and non-ST-segment myocardial infarction.8,10,11, 21-28
Myocardial infarction can occur in patients who do not have coronary
artery disease
8,24
and myocardial injury caused by CO poisoning has
been associated with an increased risk of short-term and long-term
mortality.25,29
Neurologic signs and symptoms are a prominent part of the clinical
picture of CO poisoning. Hypoxia increases intracranial pressure and
can cause cerebral edema, and these effects, along with direct cellular
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toxicity, is partially the cause of the neurologic signs and symptoms of
CO poisoning. Ataxia, dizziness, drowsiness, fatigue, headache, and
other neurologic signs and symptoms are common after CO poisoning.
More serious effects such as coma, seizures, and syncope can occur
after a moderate to severe exposure to CO.3,7,20 Other neurologic
effects such as hearing loss,30,31 peripheral neuropathy,32 amnesia,33
cataracts,34 chorea,35 tics,36 and monoparesis,37 have been reported.
Perhaps the most studied and most concerning of the neurologic
effects of CO poisoning is a phenomenon called delayed
neuropsychiatric sequelae (DNS). Some patients who have suffered CO
poisoning will develop neurological deficits after a symptom-free
period of time. Because of the seriousness of this problem and
because the risk of neurological sequelae is one of the primary reasons
for the use of hyperbaric oxygen (HBO) therapy to treat patients who
have been poisoned with CO, DNS will be discussed separately.
Delayed Neuropsychiatric Sequelae
Delayed neuropsychiatric effects are considered to be one of the most
serious complications of CO poisoning. Complete recovery is possible
and most patients do recover, but severe and permanent affective,
cognitive, and autonomic and motor impairments can also happen.

Incidence:
Delayed neuropsychiatric sequelae appear to be relatively
common, but the exact incidence of this complication is not
known. Researchers have reported incidences of 2.75%,
14.4%, 30%, 40%, and 47%,38-42 and abnormal EEGs have
been reported in 58% of patients who were diagnosed as having
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DNS.43 Different criteria used to evaluate patients, different
criteria used to define DNS, and different patient populations
probably explain why the reported incidence of DNS varies so
widely.

Onset:
The onset of DNS has been reported to be from 7-40 days after
exposure,44 6-42 days after exposure,45 and other figures have
been cited as well.

COHb levels and signs/symptoms:
There does not seem to be a correlation between COHb levels
and the development of DNS. Patients who are comatose often
do, but may not develop neuropsychiatric sequelae, and patients
who have not lost consciousness may develop serious
neurological problems.46,47
Some factors that seem to be consistently associated with an
increased risk of developing DNS are age > 36 and a duration of
exposure > 24 hours.48 Other researchers noted an association
between a duration of exposure > 6 hours, seizures, a Glasgow
Coma Score < 9, leukocytosis, and elevated CK, or a systolic
blood pressure < 90 mm Hg and DNS.41 A recent (2014) study
found that predictors for the development of delayed
encephalopathy were: abnormal CT findings that indicated
hypoxic encephalopathy; high creatine kinase; high creatinekinase MB; high lactate dehydrogenase, and; low Global
Assessment Scale score.49
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
Recovery:
Recovery from DNS is possible.50-52 The rate of recovery from
DNS has been estimated to be approximately 75%.42,53

Signs and Symptoms:
The signs and symptoms of neuropsychiatric sequelae can be
divided into affective, cognitive, and autonomic and motor
impairments. Affective impairments that have been reported
include anxiety, depression, irritability, mood swings, and
psychosis. Cognitive effects that have been reported include
deficits in attention, concentration, memory, and speech, and
dementia. Autonomic and motor impairments that have been
reported include chorea, dystonia, incontinence, myoclonus, and
parkinsonism signs such as bradykinesia, mask face rigidity,
and shuffling gait.7,44,54-56
The Toxic Dose Of Carbon Monoxide
The toxic dose of CO will depend on the patient characteristics
such as age, medical history, metabolic rate, and respiratory rate
and the environmental factors of CO concentration in the air and
the duration of exposure. The concentration of CO in the inspired
air and the duration of exposure are the factors that are most
predictive of the seriousness of the exposure. The higher the
concentration of CO and the longer the duration of the exposure,
the higher the COHb level will be.
The Occupational Safety and Health Administration (OSHA) standard is
that workers cannot be exposed in an eight hour work day to an
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average of more than 50 parts per million (ppm). Most CO detectors
that are installed in homes begin to alarm if the CO concentration in
the air averages 70 ppm for an hour or longer. Most people will begin
to experience symptoms, e.g., dizziness, headache, when the CO level
is 100 ppm, and, a CO level of 5000 ppm is usually lethal within five
minutes. Blood levels of CO do not correlate well with symptoms, but
higher levels are more likely to cause signs and symptoms, and COHb
levels 50% and higher have been associated with coma, seizures, and
death.3,57
The Carboxyhemoglobin Level
The carboxyhemoglobin level is a vital piece of information that is
needed to assess a patient who has or is suspected to have CO
poisoning. In order to use the COHb as an assessment tool you must
know: 1) if the patient smokes and if she/he does, how much; 2) the
medical problems and clinical conditions that can affect COHb level; 3)
how the COHb level was measured; 4) when the COHb level was
measured in relation to the time the patient was last exposed, and; 5)
what treatment for CO poisoning the patient has received.
The normal level of COHb is approximately 0.1-1% in non-smokers.
Tobacco combustion produces CO so smokers will have higher CO
levels than non-smokers. The typical smoker will have a COHb level of
3-5%.9 Each pack of cigarettes smoked per day will raise the COHb
level approximately 2.6%,58 and heavy smokers who have lung
disease may have a COHb level > 10%.9 There are individual
variations in COHb level, but if a non-smoker has a COHb level > 4%
or a smoker has a COHb level > 10%, CO exposure should be
suspected.9
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Patients who have hemolytic anemia, patients who have an elevated
serum bilirubin level, patients who have malaria, and patients with
sepsis or shock, can have elevated COHb levels.59-61 An elevated COHb
level has been reported in a patient who was mechanically ventilated
and receiving nitric oxide therapy.62 The accuracy of COHb levels can
be affected if the level is < 2-3%, if the blood specimen is lipemic, if
the patient has received methylene blue, or in the presence of fetal
hemoglobin.63 The issue of fetal hemoglobin and measuring COHb
levels in infants will be discussed in a separate section.
Carboxyhemoglobin levels are measured with a co-oximeter, a device
that can measure the amount of hemoglobin that is saturated with CO.
Either arterial or venous blood can be used to measure COHb.3,9 Some
types of pulse oximeters - but not all - can accurately measure COHb,
as well. Older models of pulse oximeters were not able to distinguish
between hemoglobin saturated with oxygen and COHb. However, there
are newer types of pulse oximeters that can make this distinction and
prove an accurate measurement of CO.3
Carbon monoxide is rapidly absorbed. Elimination depends on several
factors but the rate of dissociation of COHb is directly proportional to
the percentage of inhaled oxygen, so the more oxygen that can be
delivered the faster COHb will be eliminated. The half-life of CO when
someone is breathing room air is approximately 4-6 hours, the half-life
of CO is approximately 60 minutes when someone is breathing 100%
oxygen, and the half-life of CO is approximately 20 minutes if
someone is treated with hyperbaric oxygen.3 When you are
interpreting COHb levels, you must always take into account: a) how
long the patient has been away from the source, and b) how long the
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patient has been receiving oxygen and how much oxygen he/she has
been receiving.
Carboxyhemoglobin levels are needed to confirm the presence of CO
poisoning. Carboxyhemoglobin levels are also used to determine what
treatment the patient should receive, and to some degree the COHb
level may predict the level of severity of CO poisoning. However, there
is universal agreement that COHb levels are unreliable for predicting
the severity of any particular case of CO poisoning and should not be
depended upon to do so.7,14.15 Levels of 47% have been reported in
patients who have minimal symptoms, and levels of 10% have been
noted in patients who were comatose.64 Also, the level of COHb that is
used to determine what treatment the patient needs - specifically
whether or not the patient should receive hyperbaric oxygen therapy is not clear or universally agreed upon.
Treatment Of Carbon Monoxide Poisoning
Treating a case of CO poisoning begins by removing the patient from
the source, assessing the patient’s airway, breathing, and circulation
(ABCs), and assessing the patient’s cardiac and neurological status. If
the patient has suffered a cardiac arrest, is comatose, or is having a
seizure or an arrhythmia, 100% oxygen should be administered and
basic, supportive care provided. The best initial treatment for any
patient with CO poisoning is high concentration oxygen and basic
supportive care. If the patient has chronic obstructive pulmonary
disease and retains carbon dioxide, high concentrations of oxygen
should be used with caution.65 Sometime during the initial assessment
learning the circumstances of the exposure should be sought out. If
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the fire department responded to the scene, it should be determined
whether a measurement of the CO level of the air was obtained.
If the patient has normal ABCs and no serious signs and symptoms,
and there is no report of loss of conscious or seizures, the health team
should ensure that he/she is receiving 100% oxygen and start
continuous cardiac monitoring. An evaluation of the patient’s cardiac
and neurologic status should be performed. At a minimum, a 12-lead
ECG, a COHb level, and creatine-kinase MB and troponin levels should
be obtained. If the patient lost consciousness, had a seizure, or there
is other evidence of serious toxicity, an arterial blood gas (ABG), blood
urea nitrogen (BUN) and creatinine, serum electrolytes, serum lactate
level, serum CK, and urine myoglobin should be obtained. If the CO
exposure resulted from intent to cause self-harm, it’s recommended to
obtain an acetaminophen level, an ethanol level, and a salicylate level.
Computed tomography (CT) scanning or magnetic resonance imaging
(MRI) scanning of the head should be performed if the patient has any
neurological deficits.
Learning Break: Be very careful to document when the patient was
last exposed to CO, when and at what percent/flow oxygen therapy
was started, and when the COHb level was obtained. These facts will
be very important in terms of assessing the severity of the case, the
patient’s response to therapy, and the possible need for more
aggressive treatment.
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The patient should continue to receive high-concentration oxygen until
he/she is asymptomatic, the ECG is normal, myocardial injury has
been ruled out, and the COHb level is < 10%.3 If the patient has
cardiovascular or pulmonary disease, he/she should be treated until
the COHb is 2%.3 The half-life of CO is approximately 60 minutes
when a patient is breathing 100% oxygen, so patients with low levels
of COHb and mild signs and symptoms on admission to the emergency
department can often be discharged after several hours of treatment.
Before the patient is discharged, a
Mini Mental Status exam should be
The Mini Mental Status exam is
performed to screen for
performed and a follow-up
appointment for a neurologic exam
cognitive impairment, such as
to patient orientation to time
should be arranged. The Mini Mental
Status exam is a 30-question exam
and place, attentiveness,
memory, speech and the ability
that is used to detect cognitive
to follow commands.
impairments. It is popular because it
can be used quickly and easily. If cognitive deficits are detected using
this test more sophisticated neurologic testing should be done.
Additionally, the safety of the environment that the patient is returning
to should be ascertained. For example, if the patient is returning
home, it should be verified whether there are functioning CO detectors
in the residence. The patient should also be informed about how CO is
produced, and an effort made to review with the patient what is/is not
safe in terms of home heating strategies.
If the patient does not respond to normobaric oxygen (oxygen
delivered at normal atmospheric pressure), or if the patient has
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serious complications, or if the patient is considered to have a serious
exposure, two issues must be considered:
a) the patient may be suffering from cyanide exposure or
methemoglobinemia (the latter is very uncommon), or;
b) the patient may need hyperbaric oxygen (HBO) therapy.
Cyanide can be produced as a by-product of combustion that occurs
during house fires.
Patients who have suffered a serious CO poisoning should be admitted
to intensive care. There are no universally agreed upon criteria for
what constitutes a serious CO poisoning, but most clinicians would
consider the exposure to be serious if any of the following were
present.

Arrhythmias

Cardiac ischemia

COHb > 25

Loss of consciousness

Metabolic acidosis

Persistent depressed level of consciousness

Seizure

Pregnancy
Hyperbaric Oxygen Therapy
Hyperbaric oxygen therapy delivers 100% oxygen at atmospheric
pressures that are 2 to 3 times above normal, and it greatly increases
the amount of oxygen dissolved in the blood. Normally the blood
oxygen concentration is 0.3 ml/dl. When a patient is placed in an HBO
chamber at 3 times normal atmospheric pressure (3 ATM), the blood
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oxygen concentration is 6 ml/dl. The therapeutic mechanisms by which
hyperbaric oxygen work include increased dissociation of COHb,
increased plasma concentration of oxygen, increased dissociation of
CO from cytochrome oxidase, increasing free radical production, and
decreased leukocyte-mediated inflammation.23,24
Hyperbaric oxygen is routinely used for patients with serious CO
poisoning or patients who do not respond to normobaric oxygen
therapy. The goal of hyperbaric oxygen therapy is to prevent the
development and/or reduce the severity of neurological sequelae.
Hyperbaric oxygen therapy has been used for many years and is
commonly prescribed for patients with moderate to severe CO
poisoning. However, some basic issues about using it are still
controversial.

The effectiveness of hyperbaric oxygen therapy:
There is no doubt that hyperbaric oxygen has many beneficial
physiological effects and given the pathological processes of CO
poisoning, it makes sense that hyperbaric oxygen therapy would
be an effective treatment for CO poisoning. There is a lot of
evidence that hyperbaric therapy does reduce the incidence and
severity of neurological sequelae. However, when the evidence
for and against the use of HBO is examined, randomized trials do
not show that HBO prevents the development of DNS.66

Patient selection:
There are no universally accepted criteria for selecting patients
who would benefit from HBO therapy. There is no agreed upon
definition of what constitutes a serious CO poisoning, no one
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knows what level of COHb is dangerous, and there are no highly
reliable predictors that can identify which patients with CO
poisoning are at risk for developing delayed neuropsychiatric
sequelae.
The Undersea and Hyperbaric Medicine Society recommends
using CO when: 1) the patient has had a loss of conscious, even
a transient loss; 2) there are abnormal neurologic findings; 3)
the COHb level is ≥ 25%; 4) the patient is pregnant, or; 5) there
is a significant metabolic acidosis.67 These criteria are widely
known and cited, but not used by all HBO centers.
In a 2012 survey of 30 HBO treatment facilities, 19 centers used
the COHb level as an independent factor for choosing which
patients to treat, 10 centers relied solely on symptoms to decide,
4 used the COHb level as the only factor for selecting patients
for HBO therapy, and 19 centers did not have a protocol.68 A
survey of the directors of HBO treatment facilities showed similar
differences, but significant neurologic problems such as coma,
abnormal neuropsychiatric test results, and evidence of cardiac
ischemia were commonly agreed upon criteria for the use of
HBO.3

The end-point and the duration of HBO therapy:
There are no standard protocols for how often someone should
receive HBO therapy, and when it should be discontinued. The
effectiveness of HBO therapy may decrease if the patient is
treated > 6 hours after the exposure69, but it may be effective if
it is given 16 hours to 21 day after CO poisoning.70-71 Some
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hyperbaric oxygen centers will use several treatments, some use
only one, and different hyperbaric therapy centers have different
endpoints for therapy.
Hyperbaric oxygen therapy (often called a dive) is done in a chamber.
These can be small mono-place (holding a single person) chambers or
a multi-place sealed room that can accommodate one or more
patients, a ventilator, monitoring equipment, and (occasionally) a
nurse. The mono-place chamber is filled with 100% oxygen, which is
compressed to the desired atmospheric pressure. In the multi-place
chamber, the patient breathes 100% oxygen from an outside source
and the ambient air in the chamber is compressed. Most large cities
have a hyperbaric oxygen treatment center, but the initial health care
facility may be far away from an HBO treatment center. Deciding who
is stable enough to be transferred and when he/she should be
transferred should be considered very carefully.
Patients who have been intubated may need sedation and occasionally
neuromuscular paralysis during hyperbaric oxygen treatment. The cuff
of the endotracheal tube should be deflated and refilled with sterile
saline before the patient enters the chamber; the high atmospheric
pressure can collapse the cuff if it is filled with air. The patient’s
pulmonary status and blood pressure must be monitored carefully
when he/she is in the chamber. Hypercapnia can increase the risk of
seizures, so the PACO2 should be maintained at a normal level.
Hyperbaric oxygen therapy can lower the blood pressure, so blood
pressure should be checked frequently, especially if the patient has
cardiovascular disease or is receiving an intravenous vasopressor. The
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duration of most dives is about 2 hours. Some will require multiple
dives over the course of several days.
Most side effects of HBO therapy are mild and temporary. Middle ear
barotrauma such as bleeding, pain, and perforation of the eardrum is
very common72,73 with an incidence as high as 35.8% reported.72
Barotrauma to the lung and air embolization are rare adverse
effects.74,75 Seizures are possible, but they do not cause residual
damage. The incidence of seizures during hyperbaric oxygen therapy is
very low, typically < 1%.76 The presence of anxiety, fever,
hypothermia, prior seizure, traumatic brain injury and a high HBO
pressure may increase the risk of seizure occurrence during HBO
therapy.76
Children And Carbon Monoxide Poisoning
There is a relative lack about CO poisoning in the pediatric population.
Children have a higher metabolic rate and a developing nervous
system, so it seems intuitive that they would be more susceptible to
the effects of CO poisoning at lower levels of CO. However, the
published literature that discusses pediatric CO poisoning either does
not mention the issue or simply offers speculation about it. It does
appear that central nervous system effects such as lethargy and
syncope are more common in children who have CO poisoning than in
adults,77-79 and the incidence of DNS is lower for children than
adults.44,80
Significant cardiac damage in pediatric patients with CO poisoning has
been reported,81 and a 2010 study found that 16 of 107 pediatric
patients with CO poisoning had cardiac biomarkers, and
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echocardiography revealed some that had a low ejection fraction and
left ventricular dysfunction.82
The other issue specific to the pediatric patient and CO poisoning is
interference with measurement of the COHb level by the presence of
fetal hemoglobin. Fetal hemoglobin is a form of hemoglobin that has a
greater affinity for oxygen than adult hemoglobin. At birth infants have
a fetal hemoglobin concentration of approximately 70%. By age 6
months the fetal hemoglobin concentration is typically 1-2%,83
although children with sickle cell disease or thalassemia can have
higher levels. Certain methods of measuring COHb will also measure
fetal hemoglobin as COHb. The higher the level of fetal hemoglobin the
greater the degree of interference and false COHb levels as high as 78% have been reported.3,84
Carbon Monoxide Poisoning In The Pregnant Patient
Carbon monoxide can be very dangerous to a fetus because even a
relatively small decrease in maternal oxygen saturation can cause a
sharp drop in fetal oxygen saturation. In addition, fetal hemoglobin
has a higher affinity for binding to CO than maternal hemoglobin,
COHb levels in the fetus can be 10-15% higher than in the mother,
and fetal elimination of COHb is much slower than the maternal
elimination rate.85
Severe maternal carbon monoxide poisoning has been associated with
high fetal mortality rates, and serious complications such as cerebral
palsy, limb deformities, microcephaly, motor and neurological
disabilities, and mental retardation are possible.57,85,86 Fetal death and
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fetal injury can also occur even if the mother is relatively
asymptomatic.87
The recommendations for treating the pregnant patient who has CO
poisoning are essentially the same as for any other patient, but there
are several important differences. A medical toxicologist or a
hyperbaric medicine physician should be consulted in all such cases.
Administration of 100% oxygen may need to be continued for much
longer than it would normally be needed because of the COHb-fetal
hemoglobin binding and the higher fetal COHb levels. Additionally, as
pregnancy is considered to be one of the indications for the use of HBO
therapy in cases of CO poisoning, early notification of the local HBO
treatment facility would be prudent.
What If The Patient Does Not Respond To Treatment?
There are several reasons why a patient who has been poisoned with
CO does not respond to treatment, but perhaps the most common
cause of a lack of response would be cyanide poisoning. Cyanide is a
highly toxic gas that is produced when there is incomplete combustion
of nitrogen-containing material. It is a chemical asphyxiant, which
interferes with aerobic production of ATP by binding to cytochrome
oxidase and preventing the use of oxygen by the electron transport
chain, and it is a very dangerous gas.
The exact incidence of cyanide poisoning caused by fire and smoke
inhalation is not known, but it is thought to be common.88 Since these
situations (house fires, etc.) very often cause CO poisoning as well,
the patient is at great risk for hypoxic injury and there may be a
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synergistic effect between CO and cyanide that increases the toxicity
of each one.
Determining if a patient who has CO poisoning also has been poisoned
by cyanide is not simple. Cyanide poisoning should be suspected if:
1) The patient with CO poisoning caused by a fire does not
respond to oxygen therapy as expected;
2) The patient was involved in an enclosed space fire;
3) The patient has an altered level of consciousness;
4) The patient has an elevated plasma lactate level, and;
5) The patient has hypotension that cannot be explained by the
CO poisoning or by another pathologic mechanism.88
Cyanide poisoning will not respond to oxygen therapy; the pathologic
mechanism of cyanide poisoning and CO poising are distinctly
different. Patients with cyanide poisoning must be given the cyanide
antidote kit or hydroxocobalamin (an injectable form of vitamin B-12).
Patients with combined CO and cyanide poisoning may also benefit
from hyperbaric oxygen therapy but there is no evidence that proves it
is effective for cyanide poisoning. Some toxicologists and emergency
department physicians feel that hydroxocobalamin should be given
empirically to most fire victims; these patients should be evaluated on
a case-by-case basis for the use of this antidotal therapy.
Is Ambient Levels Of CO Harmful?
Carbon monoxide is a by-product of the combustion of fossil fuels and
the combustion of carbon-containing material for fuel, and it is a
common air pollutant. The ambient levels of CO in urban areas have
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been found to range from 2-40 ppm, but in areas of heavy automobile
traffic the ambient level can reach an average of 500 ppm.89 Secondhand smoke can also be a significant source of ambient CO.90
The harm that can be caused by second-hand smoke is well
documented. There is also strong evidence that chronic exposure to
ambient CO as part of air pollution increases cardiovascular morbidity
and mortality.89,91-95 The studies that have examined the health
effects of chronic exposure to CO as an air pollutant are in part
confounded by the presence of other air pollutants and varying study
group population, and the contribution of ambient CO to cardiovascular
morbidity and mortality has not yet been determined.
Follow-Up After CO Poisoning
People who have had CO poisoning should be followed closely after
discharge. People who survive CO poisoning appear to have a
significantly higher rate of death than the general population: one
study found the increase in deaths in this population to be twice what
would be expected.96 The onset of delayed neuropsychiatric sequelae
can occur weeks after an exposure to CO, so the patient and the
physician who is providing follow-up care must be aware of this. If
these complications do occur, there are no treatments that have been
evaluated with clinical trials.
Symptomatic and supportive care should be provided, and this can
include (when appropriate) occupational therapy, physical therapy,
and speech therapy. Cognitive symptoms from DNS have been treated
with donepezil (a drug used for the treatment of mild to moderate
dementia), but this is an unlabeled use of the drug, there is very little
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experience using donepezil for this purpose, and the results have been
equivocal.97-99 Hyperbaric oxygen therapy has also been used for this
purpose but again, the clinical experience is limited.100-101
Stimulant drugs such as dextroamphetamine, methylphenidate, and
modafanil might be helpful to treat attention and memory deficits, but
there is no clinical experience with them as yet. If the patient has
signs and symptoms of Parkinsonism, standard therapy with
anticholinergics and levodopa can be used, but as with the other
pharmacological therapies mentioned, there is very little clinical
experience and the results have been equivocal.102
Summary
Carbon monoxide is a dangerous gas that is produced by the
incomplete combustion of fossil fuels such as gasoline and kerosene,
and by the combustion of carbon-containing materials like coal and
wood. Carbon monoxide is also produced endogenously and by burning
of tobacco. The normal COHb level for a non-smoker is usually ≤ 1%
and for a smoker it is 3-5%. Poisoning with CO occurs when the gas is
inhaled, and CO causes harm by two basic mechanisms: 1)
preferentially binding hemoglobin, thus causing tissue hypoxia, and; 2)
direct cellular toxic mechanisms. The result of CO poisoning is
decreased oxygen delivery and disruption of cellular metabolism.
The signs and symptoms of CO poisoning are vague and non-specific.
However, CO has the strongest effect on the organs that are the most
metabolically active and have high oxygen demands, so the brain and
the heart are the most vulnerable to CO. Cardiac and neurologic signs
and symptoms predominate in cases of CO poisoning. These can be
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mild and self-limiting or quite serious. Most patients will complain of
headache, dizziness, and palpitations, but coma, myocardial infarction,
permanent neurological deficits, seizures and death are possible. A
particularly concerning effect of CO poisoning is delayed
neuropsychiatric sequelae (DNS). Some patients who have suffered CO
poisoning will have an asymptomatic period of days to weeks and then
will develop debilitating affective, cognitive, and autonomic/motor
deficits.
Treating CO poisoning begins with understanding the circumstances
and situations in which CO poisoning is likely. These may not always
be obvious or reported by the patient, and studies have shown that
occult CO poisonings, poisonings in which CO was not initially
identified as the cause of the patient’s complaints, are relatively
common.103-104 Treatment of confirmed cases of CO poisoning always
begins with assessment and stabilization of the ABCs, administration
of 100% oxygen, and continuous cardiac monitoring.
Diagnostic and laboratory test should include a COHb level, creatine
kinase MB and troponin levels, and a 12-lead ECG. Other tests that
may be needed will depend on the patient’s condition and may include
an ABG, BUN and creatinine, serum electrolytes, serum CK, serum
lactate level, urine myoglobin level, and CT or other scanning of the
head. A thorough assessment of the patient’s neurological and
cardiovascular status should be done as well. The COHb level is a vital
part of the assessment, but COHb levels do not accurately predict the
seriousness of the exposure.
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Patients should receive supplemental oxygen and be observed for at
least four to six hours, and most patients can be discharged when the
COHb level is < 10and the signs and symptoms have resolved. A Mini
Mental Status exam should be performed before the patient leaves the
emergency department. In addition, the health team should make sure
that the patient understands how CO poisoning happens and, if he/she
is returning home, that there are functioning CO detectors at the
residence. A follow-up appointment for a neurologic exam should be
arranged.
If the patient has had serious signs of symptom of CO poisoning,
normobaric oxygen may not be sufficient and HBO may be indicated.
There are no universally accepted criteria for when to use HBO and for
whom, but the commonly cited indications for HBO are: 1) the patient
has had a loss of conscious, even a transient loss; 2) there are
abnormal neurologic findings; 3) the COHb level is ≥ 25%; 4) the
patient is pregnant, or; 5) there is a significant metabolic acidosis.
Hyperbaric oxygen therapy is primarily used to prevent the
development of DNS. However, despite many years of clinical
experience and much study, the clinical benefits of HBO therapy for
the prevention of DNS are still unproven.
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1.
Carbon monoxide is produced by:
a. incomplete combustion of carbon-containing fuel
b. combustion of nitrogen-containing materials
c. vapors emitted from carbon-containing fuel
d. combustion of in organic acids
2.
Carbon monoxide can also be produced by:
a. toluene
b. methylene chloride
c. cyanide
d. cadmium
3.
One of the basic ways by which CO causes harm is:
a. decreased production of hemoglobin
b. production of abnormal hemoglobin
c. tissue hypoxia
d. pulmonary and coronary vasoconstriction
4.
One of the basic ways by which CO causes harm is:
a. damage to pulmonary capillaries
b. production of methemoglobin
c. hemolysis
d. direct cellular toxicity
5.
Two organs particularly vulnerable to CO poisoning are:
a. the brain and the heart
b. the kidneys and the pancreas
c. the thyroid gland and the small bowel
d. the lungs and the liver
6.
True or false: COHb level is a good predictor of the
seriousness of the CO exposure.
a. True
b. False
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7.
The primary treatment for CO poisoning is:
a. hydroxocobalamin
b. 100% oxygen
c. endotracheal intubation
d. methylene blue
8.
Patients who have had CO poisoning are at risk for:
a. delayed neuropsychiatric sequelae
b. increased risk of developing metabolic syndrome
c. delayed onset of liver damage
d. increased risk of developing Alzheimer’s
9.
Which of the following are indications for the use of HBO?
a. Age < 5 years, COHb level > 10%
b. Pregnancy, COHb level ≥ 25%
c. Age > 55 years, headache
d. Female gender, metabolic acidosis
10. The primary use of HBO is to prevent:
a. the development of delayed myocardial ischemia
b. the development of shock to the liver
c. the development of rhabdomyolysis
d. the development of delayed neuropsychiatric sequelae
Correct Answers:
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
A
B
C
D
A
B
B
A
B
D
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