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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 nonspecific 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 during 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 3 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 exposures and
the standard treatments for carbon monoxide 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 (CO) is a gas that is
a.
b.
c.
d.
colorless.
smells similar to car exhaust.
taste similar to ammonia.
All of the above
2. Carbon monoxide (CO) can be produced by
a.
b.
c.
d.
toluene
methylene chloride
cyanide
cadmium
3. One of the basic ways carbon monoxide (CO) causes harm is
a.
b.
c.
d.
it
it
it
it
decreases production of hemoglobin.
produces abnormal hemoglobin.
causes tissue hypoxia.
causes pulmonary or coronary vasoconstriction.
4. Carbon monoxide (CO) can cause
a.
b.
c.
d.
pulmonary capillary vasoconstriction.
production of methemoglobin.
hemolysis.
direct cellular toxicity.
5. Two organs particularly vulnerable to CO poisoning are
a.
b.
c.
d.
the
the
the
the
brain and the heart.
kidneys and the pancreas.
thyroid gland and the small bowel.
lungs and the liver.
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Introduction
Carbon monoxide 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 carbon
monoxide (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 Of Carbon Monoxide Poisoning
Carbon monoxide poisoning is still very common, and is a leading
cause of morbidity and mortality in the United States.1 Each year a
minimum of 50,000 people who have been exposed to CO present to
hospital emergency rooms and the estimated number of visits because
of CO poisoning is much higher;2,3 in 2014 there were 1319 deaths
caused by CO;4 and, large-scale CO caused by environmental factors
are relatively common.5,6 Exposures to CO can happen at any time of
the year but are more common in the winter. If temperatures are very
cold and/or there is a power outage, people may attempt to heat their
homes in unsafe ways. In late October of 2011 in Connecticut, a heavy
snowstorm caused widespread power outages, and ambient
temperatures at the time were unusually low. Emergency rooms in the
state were inundated with cases of carbon monoxide poisoning caused
by indoor use of gasoline generators and charcoal burning grills.6
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Carbon monoxide is produced when carbon-containing materials such
as coal, oil, tobacco, or wood are burned. Common sources of CO
exposures that can cause poisoning are automobile exhaust fumes,
fumes from any gasoline powered engine, natural gas, and wood fires.
It is important to remember that CO poisonings happen because of the
production of CO that occurs when the source material is burned and
when these combustion fumes are not properly ventilated.
Two other exogenous sources of carbon monoxide are methylene
chloride and methylene iodide. Methylene chloride is a chemical that is
a common 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
exposure.7 Methylene iodide is used by jewelers to examine gems and,
like methylene chloride, it is converted in vivo to CO.8 Carbon
monoxide poisoning caused by either of these is very uncommon;
there has only been thirteen reported cases of methylene iodide
poisoning.9,10
Carbon monoxide is also an endogenous compound. It is produced by
the breakdown of hemoglobin, lipid peroxidation, and the metabolism
of xenobiotics (substances foreign to the body), and it functions as an
intrinsic signaling molecule that influences cell functioning proximally
and distally.11,12 The normal level of carbon monoxide in the blood,
which is carboxyhemoglobin (COHb) is 0.1%-1.0%, although it may be
higher (carboxyhemoglobin levels are discussed later in this course).
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Although the concept is in the experimental stages, in vitro and animal
research suggests that carbon monoxide may have therapeutic
value.13,14
Carbon Monoxide Poisoning: Pathophysiology
The mechanism by which CO was traditionally thought to cause
poisoning was by its binding to hemoglobin. This is certainly one of the
ways that CO causes harm, as will be discussed in detail later in this
section. But research has shown that CO poisoning is much more
complex and there are multiple, dynamic pathologic processes
involved in CO poisoning. As Tomaszewski wrote: “CO toxicity cannot
be attributed solely to COHb-mediated hypoxia. Neither the clinical
effects nor the phenomena of delayed neurologic deficits can be
completely predicted by the extent of binding between hemoglobin and
CO.”1
The pathophysiologic mechanisms of CO poisoning are briefly reviewed
below.1,2,15-21 Some of these are well outlined and their role in CO
poisoning is known while others are more theoretical in nature, and
many are interdependent but they are discussed separately for ease of
understanding.
Hemoglobin Binding and Oxygen Transfer Effects
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
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does not bind with oxygen, so most of the hemoglobin is rendered
functionally useless.
The oxyhemoglobin dissociation curve indicates how saturated
hemoglobin is at any level of oxygen tension of the blood.
(Oxygen tension refers to the partial pressure of oxygen, which said
another way, is the pressure of oxygen in a mixture of gases). The
oxyhemoglobin dissociation curve also indicates how tightly
hemoglobin holds on to oxygen and how easily it releases oxygen for
transfer to the tissues. Saturated hemoglobin levels are plotted on a
vertical axis, and the prevailing oxygen tension on a horizontal axis to
create the oxyhemoglobin dissociation curve. Carbon monoxide shifts
the oxyhemoglobin dissociation curve to the left so for any level of
oxygen saturation less oxygen will be transferred to the tissues. This
happens for two reasons. First, carbon monoxide increases the affinity
hemoglobin has for oxygen and this prevents the release of oxygen.
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.
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.
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Cellular Effects
Carbon monoxide binds with mitochondrial cytochrome oxidase.
Mitochondrial cytochrome oxidase is 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.
High levels of nitric oxide initiate the formation of free radicals. The
tissue damage that is caused by poor perfusion stimulates an
inflammatory response and free radical formation. The result is a
reperfusion injury, caused by the return of oxygen in the blood, which
can affect the brain and other parts of the central nervous system.
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.
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 is the process of programmed cell death. Carbon monoxide
poisoning is thought to accelerate the process of apoptosis.
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Cardiovascular Effects
Carbon monoxide is thought to at times produce a catecholamine
surge and this can cause what is called myocardial stunning, which is a
temporary, non-ischemic ventricular dysfunction. Carbon monoxide
can also inhibit or impair fibrinolysis and increase the amount of
thrombin that is formed. Thromboembolic complications caused by CO
poisoning have been reported.
Carbon monoxide increases the formation of cyclic guanosine
monophosphate. Cyclic guanosine is a second messenger like cyclic
adenosine monophosphate (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.
Pathologic Mechanisms And Clinical Picture Of CO Poisoning
The individual contribution of each of these pathologic mechanisms has
not been completely clarified, and it is not understood exactly how and
why CO produces the signs and symptoms of CO poisoning. Tissue
hypoxia and decreased oxygen utilization at the cellular level are
probably responsible for the immediate signs and symptoms of CO
poisoning, but carboxyhemoglobin (COHb) levels that reflect tissue
hypoxia do not always correlate with the severity of signs and
symptoms.1,22,23 Evidence supporting this is that 1) patients do not
always improve as CO is eliminated, 2) levels of COHb that are
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considered harmless may cause cognitive impairment, and 3) 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.1,22,24
Clinical Care For Patients With Carbon Monoxide Poisoning
Are you a clinician caring for a patient who has CO poisoning? This
question may seem odd because the situation and the patient’s
complaints quite often make it obvious that a CO exposure has
occurred. For example, the patient often reports that the home heating
system malfunctioned, the CO detector was alarming, and the patient
has common signs and symptoms of CO poisoning. But the clinician
needs to remember that 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 and which prompt a
patient to seek medical attention, are relatively common; and, CO
poisoning frequently produces a clinical picture that is vague and
nonspecific. 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
aware of circumstances and situations that are likely to cause
exposure to CO.
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If CO poisoning is suspected, the clinician evaluating the patient
should ask 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 everyone in the house is ill, did his or her
symptoms begin at the same time? (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 live in a single-family home or a multi-resident building?
Research has shown that CO can diffuse through walls so the
absence of a CO producing source in someone’s personal living
space does not rule out the possibility of a CO exposure.

Do you have CO detectors and, if is so, was there an alarm
sounding?

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?
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
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? For example, is he/she a mechanic working in a
poorly ventilated garage, or working inside a building where gaspowered or gasoline-powered machinery is operating?

Has the patient been stripping furniture in an unventilated area?

If there is more than one patient and everyone has essentially
the same signs and symptoms, determine if all 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; if it
was the latter, the issue may be an infectious illness.
Signs And Symptoms Of Carbon Monoxide Poisoning
Carbon monoxide poisoning can be
difficult to detect because the symptoms
may be mild and they are nonspecific.
Also, the number and intensity of the
signs and symptoms of CO poisoning is
If there is no obvious or
known exposure to CO, a mild
CO exposure can be
overlooked or misdiagnosed.
not always related to the COHB level (COHb levels are discussed in
detail in a later section).1,22,23 Patients with low levels may be sicker
than patients with high levels.
However, despite the complexity of CO poisoning and the nonspecific
nature of the signs and symptoms, the clinical presentation of CO
poisoning is easily understood by remembering these three points. The
basic underpinnings of CO poisoning are: 1) Decreased oxygen
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delivery, 2) Decreased oxygen utilization, and 3) Direct toxic injuries
to vulnerable tissues. Keeping these three things in mind, it is
relatively simple to understand how CO poisoning presents and why
certain populations are vulnerable.
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.1 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 serious CO poisoning than do healthy
individuals or those who are neither very young nor very old.
CO Symptom Severity
The severity of CO poisoning depends on patient risk factors and on
the circumstances of the exposure, but essentially the higher the CO
level and the longer the time of exposure then the sicker the patient is
likely to be.
The clinical picture of CO poisoning can be usefully divided into mild,
moderate, and severe. 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.
Patients with mild CO may have confusion, dizziness, fatigue,
headache, nausea, and tachycardia. Patients with moderate CO
poisoning may have ataxia, chest pain, dyspnea, syncope, and
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tachycardia. And, patients with severe CO poisoning may have
arrhythmias, coma, hypotension, metabolic acidosis, and seizures.
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,
nonspecific ST segment and T wave changes, pulmonary edema, and
ST-segment and non-ST-segment myocardial infarction.1,16,18,19,25-33
Myocardial injury is relatively common after CO poisoning.33,34 STsegment MI is a rare consequence of CO poisoning,16,25,35 and
myocardial infarction can occur in patients who do not have coronary
artery disease.16 Also, myocardial injury caused by CO poisoning has
been associated with an increased risk of short-term (but not longterm) mortality.23,25,29
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
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, cortical blindness, seizures, and
syncope can occur after a moderate to severe exposure to CO.1,2,36
Other neurologic effects such as hearing loss,37,38 peripheral
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neuropathy,37 amnesia,39 cataracts,40 chorea,41 tics,42 and
monoparesis,43 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. 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
A neurological condition known as delayed neuropsychiatric sequelae
(DNS) is among the most serious complications of CO poisoning. These
neurological complications occur after a period of normal
consciousness and although complete recovery from DNS is possible,
permanent, severe affective disorders, cognitive, and autonomic and
motor impairments can also happen.
Incidence of DNS
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%, 16.5%, 30%, 40%, and
47%,45-50 and abnormal electroencephalograms (EEGs) have been
reported in 58% of patients who were diagnosed as having DNS.51
Different evaluation criteria, diagnostic criteria, and patient
populations could explain why the reported incidence of DNS varies so
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widely. Hampson (2015) estimated that each year approximately 6600
people exposed to CO develop long-term cognitive sequlae.51
Onset of DNS
The onset of DNS has been reported to be from two days to eight
months after exposure.1,44
Loss of Consciousness and DNS
There is no correlation between COHb levels and the development of
DNS. Patients who are comatose after a CO exposure may, or may not
develop DNS, and patients who have not lost consciousness may
develop serious neurological problems.36,53
DNS Risk Factors
Some factors that seem to be consistently associated with an
increased risk of developing DNS are age > 36 years and a duration of
exposure > 24 hours.54 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.47 A recent (2014) study found that predictors
for the development of delayed encephalopathy were 1) abnormal
computed tomography (CT) scan findings that indicated hypoxic
encephalopathy, 2) high creatine kinase, 3) high creatine-kinase MB,
4) high lactate dehydrogenase, and 5) low Global Assessment Scale
score.47
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Signs and Symptoms of DNS
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.1,15,57-59
Recovery from DNS
Recovery from DNS does occur,55,56 and the rate of recovery is quite
variable, from 56% to 97%.1
The Toxic Dose 0f Carbon Monoxide
The toxic dose of carbon monoxide depends on patient characteristics
of 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 and the greater the risk for harm.
The Occupational Safety and Health Administration (OSHA) standard is
that workers cannot be exposed in an eight-hour working day to an
average of more than 50 parts per million (ppm) of CO. Most Carbon
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monoxide detectors installed in private residences are usually
calibrated to alarm if the CO concentration in the air averages 70 ppm
for an hour or longer. Most people will begin to experience symptoms,
such as, dizziness and 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.60
Carboxyhemoglobin Level
The carboxyhemoglobin (COHb) 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 for assessment the clinician must
know: 1) If the patient smokes and, if so, how much, 2) 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.
COHb Level and Smoking
Tobacco combustion produces CO and smokers have higher COHb
levels than nonsmokers. Smokers typically have COHb levels of 6%10%61-63 and higher levels have been reported.63,64 Each pack of
cigarettes smoked per day will raise the COHb level approximately
2.6%,65 and in moderate and heavy smokers a single cigarette will
significantly increase the COHb level for six hours or longer.66
A COHb level of > 3% in a non-smoker or > 10% in a smoker is
strongly suggestive of a CO exposure.15
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Medical Problems and Clinical Conditions and COHb Level
Hemolytic anemia, sickle cell disease, an elevated serum bilirubin level
with hemolysis, malaria, and trauma can cause an elevated COHb
level.67-72 An elevated COHb level has been reported in a patient who
was mechanically ventilated and receiving nitric oxide therapy.73
The accuracy of COHb levels can be affected if the COHb level is
< 2%-3%, if the blood specimen is lipemic, if the patient has received
methylene blue, or in the presence of fetal hemoglobin.74
The patient’s medical conditions and age need to be considered as well
when interpreting COHb levels. A patient who has anemia,
cardiovascular disease, or pulmonary disease will be vulnerable to
decreased oxygen delivery and utilization. Children and infants may be
particularly vulnerable to CO poisoning because of their higher
metabolic rate; because they cannot accurately – or cannot at all – tell
someone how they feel; and, because of the presence of fetal
hemoglobin.75
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%; this ratio is rapidly
reversed by three to six months of age, and at one year fetal
hemoglobin is essentially gone.74,76 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 in
the presence of fetal hemoglobin, false COHb levels as high as 7% to
8% have been reported.1,76
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Measurement Techniques and COHb Levels
Carboxyhemoglobin levels are measured with a co-oximeter, which is 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.1, 23 Older bedside pulse oximeters were not able to distinguish
between hemoglobin saturated with oxygen and COHb.1 Bedside pulse
co-oximeters have shown some promise as a screening device but
their accuracy at specific levels and in certain clinical conditions has
been questioned.1,44,77-79 A recent 2017 literature review by a
subcommittee of the American College of Emergency Physicians
(ACEP) recommended against using bedside pulse co-oximeters for
diagnosing CO poisoning.80
Carbon Monoxide Absorption and Elimination
Carbon monoxide is rapidly absorbed. Elimination depends on several
factors but increasing the partial pressure of oxygen increases the rate
of dissociation of COHb so the more supplemental oxygen that is
delivered, the faster COHb will be eliminated. The half-life of COHb
when someone is breathing room air is approximately 4-6 hours, and it
is approximately 60 minutes when 100% oxygen is applied. The halflife of COHb is reduced to approximately 20 minutes if someone is
treated with hyperbaric oxygen.1,2,36,44 When a clinician is interpreting
COHb levels, he/she must consider how long the patient has been
away from the source of CO, and how long and how much oxygen the
patient had received.
Carboxyhemoglobin levels are needed to confirm the presence of CO
poisoning. Carboxyhemoglobin levels are also used to determine what
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treatment the patient needs 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.1,15,22
Levels of 47% have been reported in patients who have minimal
symptoms, and levels of 10% have been noted in patients who were
comatose.81 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.
Following removal from the source and after a rapid assessment of the
ABCs, oxygen at 100% via a facemask should be applied; if the patient
is comatose, he or she should be endotracheally intubated.44 If the
patient has chronic obstructive pulmonary disease and retains carbon
dioxide, high concentrations of oxygen should be used with caution.81
Arrhythmias, hypotension, and seizures would be treated with basic,
supportive care.
Sometime during the initial assessment, the circumstances of the
exposure should be determined, i.e., how the exposure occurred, the
duration of the exposure, when the patient(s) were removed from the
source, and when oxygen was applied. If the fire department
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responded to the scene, the clinician should find out if the ambient air
concentration of CO was measured and, if so, the level of measure.
A COHb level should be done and if there is any risk for myocardial
ischemia or damage, the patient should be placed on continuous
electrocardiogram (ECG) monitoring, a 12-lead ECG should be done,
and creatine-kinase (CK) MB and troponin levels should be obtained. If
the patient has lost consciousness, has an altered level of
consciousness, had a seizure, or was hypotensive, or is at risk for
acidosis, laboratory tests of an arterial blood gas (ABG), serum lactate
level, serum electrolytes, BUN, creatinine, and serum creatinine kinase
(CK) should be measured. Computed tomography scanning or
magnetic resonance imaging (MRI) scanning of the head should be
performed if the patient has neurological deficits or lost consciousness.
If the CO exposure resulted from intent to cause self-harm, the
clinician should request laboratory testing of acetaminophen, ethanol,
and salicylate levels.
Assessment Plan for a CO Exposure
Remove the patient from the source
Apply supplemental oxygen via a face mask at 100%. Document
when this was started
Assess the ABCs
Determine the circumstances of the exposure.
Measure a COHb level
Risk for or evidence of myocardial ischemia/damage: Continuous
ECG monitoring, 12-lead ECG, CK-MB, troponin level
Acidosis, altered consciousness, hypotension or seizure: ABG,
serum lactate level, serum electrolytes, BUN, creatinine, and CK
should be measured
CO poisoning caused by self-harm: Measure acetaminophen,
ethanol, and salicylate levels
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Patients who were asymptomatic on arrival or had mild to moderate
poisoning should receive supplemental oxygen until symptoms have
resolved, and they can be discharged when it is certain that
myocardial and neurological injuries did not occur and the COHb level
has returned to normal. In most cases, four to six hours of oxygen
therapy is sufficient.
It can not be overemphasized that the clinician evaluating a patient
with possible CO poisoning should 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. Prior to discharge, the clinician should
make sure that the patient knows how and why the poisoning occurred
and to make sure the patient is returning to a safe environment.
Health clinicians understand how CO is produced but the patient may
not. The patient may return home and continue to use a
malfunctioning heating system or neglect to purchase a CO detector. A
short review about safe home heating practices is a helpful preventive
measure. In addition, before the patient is discharged, consideration
should be given to perform a Mini Mental Status Exam (MMSE) and if
needed an arrangement for a followup neurologic examination. The Mini
Mental Status Exam is a 30-question
exam that is used to detect cognitive
impairments, and it is widely used
The Mini Mental Status exam is
performed to screen for
cognitive impairment, such as to
patient orientation to time and
place, attentiveness, memory,
speech and the ability to follow
commands.
because it is quick and simple to do. If cognitive deficits are detected
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using the MMSE then more sophisticated neurologic testing should be
done. If the patient does not respond to norm-baric oxygen (oxygen
delivered at normal atmospheric pressure), if the patient has serious
complications, or if the patient is considered to have a serious
exposure, two issues must be considered: 1) the patient may be
suffering from cyanide exposure or methemoglobinemia (the latter is
very uncommon); or, 2) the patient may need hyperbaric oxygen
(HBO) therapy. Cyanide can be produced as a byproduct of
combustion that occurs during house fires (cyanide poisoning
complicating a CO exposure will be discussed in a later section).
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 an exposure to be serious if any of indicators in the Table
below is present.
Indicators of Serious CO Exposure
Arrhythmias
Cardiac ischemia
COHb > 25
Fetal distress
Loss of consciousness
Metabolic acidosis
Persistent depressed level of consciousness
Pregnancy and a COHb level of >15%
Seizure
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Patients for whom any of these indicators of CO poisoning apply should
be admitted and a toxicologist, a poison control center, or a hyperbaric
medicine specialist should be consulted.
Hyperbaric Oxygen Therapy
Patients who have serious CO poisoning are potential candidates for
hyperbaric oxygen (HBO) therapy. Hyperbaric oxygen therapy delivers
100% oxygen at atmospheric pressures that are 2 to 3 times above
normal. The dissolved concentration of blood oxygen concentration is
typically 0.3 mL/dL, but when HBO at three times normal atmospheric
pressure (3 ATM) is administered the dissolved blood oxygen
concentration is increased to 6 mL/dL. The increased plasma
concentration of oxygen is beneficial, and HBO also increases the
dissociation of CO from hemoglobin, increases the dissociation of CO
from cytochrome oxidase, and decreases free radical production and
leukocyte-mediated inflammation.2,83-85
Hyperbaric oxygen is routinely used for patients with serious CO
poisoning or patients who do not respond to normo-baric oxygen
therapy, and most often to prevent the development and/or reduce
the severity of DNS. However, important basic issues about its use
have not been clarified or resolved.
Effectiveness of Hyperbaric Oxygen Therapy
Hyperbaric oxygen therapy has many beneficial physiological effects
and given the pathological processes of CO poisoning, it seems logical
that HBO would be an effective treatment for CO poisoning,
particularly for preventing DNS. There is evidence that supports it use
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for this
86,87
and there are many HBO advocates. However, there is no
unequivocal proof that HBO can prevent DNS or reduce its severity.
There is research and literature reviews that have determined that
HBO is not an effective treatment;88 and, the American College of
Emergency Physicians (ACEP) concluded that “It remains unclear
whether HBO2 therapy is superior to normo-baric oxygen therapy for
improving long-term neurocognitive outcomes.”80
Patient Selection for Hyperbaric Oxygen Therapy
There are no universally accepted criteria for selecting patients who
would benefit from HBO therapy,89,90 and developing these criteria has
been problematic for several reasons. First, there is no agreed upon
definition of what constitutes a serious CO poisoning. Second, the level
of CO that defines a serious CO poisoning – and that would prompt the
use of HBO therapy – is not known and varies with each case. Third,
there is no reliable way to predict which patients with CO poisoning are
at risk for developing delayed neuropsychiatric sequelae. However,
HBO therapy is frequently used for cases of CO poisoning and the
recommendations for HBO do not vary significantly from source to
source. Examples are provided in the Tables below.
Undersea and Hyperbaric Medicine Society Recommendations for HBO
Therapy91
Loss of consciousness, even a transient loss
Abnormal neurologic findings
COHb level is ≥ 25%
Pregnant patients
There is a significant metabolic acidosis.
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Recommendations for HBO therapy cited by Maloney81
Carboxyhemoglobin >25%
Confusion/altered mental status
Coma
Evidence of acute myocardial ischemia
Focal neurologic deficit
Pregnancy with carboxyhemoglobin level >15%
Seizure
Syncope
Recommendations for HBO Therapy by Clardy, et al.44
COHb > 25%
Evidence of ongoing end-organ ischemia such as metabolic acidosis or
myocardial ischemia
Loss of consciousness
Pregnancy and a COHb > 20% or signs of fetal distress
Duration and End-point Number of HBO Therapy Sessions
There are no standard protocols for how often someone should receive
HBO therapy, when it should be discontinued and the duration of an
HBO therapy session. Hyperbaric oxygen therapy is thought to be
most effective when it is started within six hours of CO exposure,44
and Clardy, et al. noted that: “Benefit for patients treated more than
12 hours after their CO exposure is unproven.”44 However, there are
multiple accounts in the literature that document the benefits of HBO
therapy when it is administered days, months, and years after the
initial CO exposure,92-95 and it appears that HBO treatment will use
several treatments and have different endpoints for therapy.
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Hyperbaric Oxygen Therapy Sessions
An HBO therapy session (which is often called a dive) is done in an
HBO 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
referring health facility may be far away from the 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
duration of most dives is about 2 hours. Some patients will be
prescribed several sessions over the course of several days.
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Side Effects/Adverse Outcomes of HBO Therapy
Most side effects of HBO therapy are mild and temporary. Middle ear
barotrauma such as bleeding, pain, and perforation of the eardrum is
the most common side effect of HBO therapy96,97 with a reported
incidence as high as 10.3% - 35.8%.98,99 Factors that increase the risk
of middle ear barotrauma during HBO therapy are age (very young
and very old), the use of sedation during the HBO session, history of
ear, nose and throat (ENT) radiation, history of cardiovascular disease,
endotracheal intubation and mechanical ventilation, inflammatory
processes in the nasopharynx, and anticoagulant use.96,99 Barotrauma
to the lung and air embolization are rare adverse effects.100,101
Seizures are possible, but they do not cause residual damage. The
incidence of seizures during hyperbaric oxygen therapy is very low,
typically < 1%.102-104 The presence of anxiety, fever, hypothermia,
prior seizure, traumatic brain injury (TBI) and high HBO pressure may
increase the risk of seizure occurrence during HBO therapy.102-104 The
only absolute contraindication to using HBO is pneumothorax.
Relative contraindications include asymptomatic pulmonary blebs or
bullae seen on chest X-ray, claustrophobia, obstructive lung disease,
recent ear or thoracic surgery, uncontrolled fever, or upper respiratory
or sinus infections.
Pediatric Carbon Monoxide Poisoning
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. Central nervous
system effects of CO poisoning such as lethargy and syncope are more
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common in children than in adults,105 but DNS is less common for
children; the reported incidence of this complication has been 3% 17%,44 but a more recent study in 2016 found a 33.3% incidence of
DNS in pediatric CO poisonings.106 Permanent neurologic sequelae can
occur in children, as well.106
Significant cardiac damage in pediatric patients with CO poisoning can
occur.107 A 2010 study found that 16 of 107 pediatric patients with CO
poisoning had cardiac biomarkers indicating myocardial damage, and
evidence of ventricular wall abnormalities, and low ejection fraction,108
which were findings that were mirrored in a later study in 2016.109
If HBO therapy is necessary for a child who has CO poisoning, there
are specific issues to keep in mind.44

If the child is < five years old, has otitis media, and cannot equalize
middle ear pressure, a myringotomy should be performed.

Children may need a parent to accompany them in the HBO
chamber.

When HBO is administered to an infant, the infant should be kept
warm; hypothermia is a risk for this age group.

Certain congenital abnormalities can complicate HBO therapy. A
chest X-ray should be done to be sure the child does not have lobar
emphysema; this could cause a pneumothorax during HBO therapy.

Children who have unpalliated ductal dependent cardiac lesions
should be treated very cautiously because HBO therapy can cause
duct closure. These patients may not be suitable candidates for
HBO; and a pediatric cardiologist should be consulted.
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Carbon Monoxide Poisoning And 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 and
fetal elimination of COHb is much slower than the maternal elimination
rate.44,110
There is little published information about CO poisoning in pregnant
women. Friedman, et al. reviewed the medical literature from 1970 to
2010 and located 19 articles,110 and the largest cases series was by
Koren, et al. in 1991, examining CO poisoning in 32 patients.111 Koren,
et al. found that mild to moderate CO poisoning did not cause physical
or neurobehavioral damage but that in five cases of significant
maternal exposure there were two fetal deaths and one case of
cerebral palsy.111 Fetal morbidities associated with maternal CO
poisoning include flexia, cardiomegaly, hypotonia, hypoxic ischemic
encephalopathy, limb malformations, microcephaly, persistent
seizures, preterm delivery, and death.110 Fetal death and fetal injury
can also occur even if the mother is relatively asymptomatic and the
COHb level is low.112,113
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
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pregnancy is an indication for the use of HBO therapy in cases of CO
poisoning, early notification of the local HBO treatment facility would
be prudent. There is very little information on the effects of HBO
therapy of the fetus but it appears to be safe.44
Patient Non-Response To Oxygen Treatment
There are several reasons why a patient who has been poisoned with
CO does not respond to treatment, but perhaps the most common
reason may be cyanide poisoning. Cyanide is a highly toxic gas that
results from the incomplete combustion of nitrogen-containing
material, and cyanide gas exposure is thought to be common during
fires and smoke inhalation.2,114
Cyanide is a chemical asphyxiant, and it interferes with aerobic
production of ATP by binding to cytochrome oxidase and preventing
the use of oxygen by the electron transport chain. Since situations
such as house fires very often cause CO poisoning, the patient is at
great risk for hypoxic injury and there may be a synergistic effect
between CO and cyanide that increases their respective toxicity.
Determining if a patient who has CO poisoning also has been poisoned
by cyanide is not simple. Cyanide poisoning should be suspected if the
patient:114

with CO poisoning caused by a fire does not respond to oxygen
therapy as expected.

was involved in an enclosed space during a fire.

has an altered level of consciousness.

has an elevated plasma lactate level.
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
has hypotension that cannot be explained by the CO poisoning or
by another pathologic mechanism.
Cyanide poisoning will not respond to oxygen therapy; the pathologic
mechanism of cyanide poisoning and CO poisoning 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 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.
Are Ambient Levels Of Carbon Monoxide 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
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.115 Secondhand smoke can also be a significant source of ambient CO,116,117 and
there is also strong evidence that chronic exposure to ambient CO as
part of air pollution increases cardiovascular morbidity and
mortality.118 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
populations, and the exact contribution of ambient CO to
cardiovascular morbidity and mortality has not yet been determined.
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Follow-Up After CO Poisoning
People who have had CO poisoning should be followed closely after
discharge. Survivors of 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.119
The onset of delayed neuropsychiatric sequelae can occur weeks after
an exposure to CO, so the patient and the clinician 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, very little
experience using donepezil for this purpose exists, and the results
have been equivocal.120-122
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 yet. Anticholinergics,
aripiprazole, bromocriptine, levodopa, and levothyroxine have been
used for Parkinsonism caused by CO but there is very little clinical
experience with this approach.123-126
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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 nonsmoker is usually ≤ 1%
and for a smoker it is 6% to 10%. 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 these two basic
pathologic mechanisms is decreased oxygen delivery and disruption of
cellular metabolism.
The signs and symptoms of CO poisoning are vague and nonspecific,
but CO is the most toxic to the organs that are the most metabolically
active and have high oxygen demands, so the brain and the heart are
particularly vulnerable to CO. Cardiac and neurologic signs and
symptoms predominate in cases of CO poisoning. These can be 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 likely occurs. These may not
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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.127 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 tests 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 have been
discussed. A thorough assessment of the patient’s neurological and
cardiovascular status should be done. The COHb level is a vital part of
the assessment, but COHb levels do not accurately predict the
seriousness of the exposure or correlate well with signs and
symptoms.
Patients should receive supplemental oxygen at 100% via face mask
and be observed for at least four to six hours, and most patients can
be discharged from the hospital emergency department when the
COHb level has returned to normal and 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 or symptoms of CO poisoning, admission to the hospital
Intensive Care Unit is advised and HBO therapy may be indicated.
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There are no universally accepted criteria for when to use HBO and for
whom, but commonly cited indications for HBO raised in this course
involving serious CO exposure should prompt the treating clinician to
consult with a hyperbaric medicine specialist, a poison control center,
or a toxicologist. 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 (CO) is a gas that is
a.
b.
c.
d.
colorless.
smells similar to car exhaust.
taste similar to ammonia.
All of the above
2. Carbon monoxide (CO) can be produced by
a.
b.
c.
d.
toluene
methylene chloride
cyanide
cadmium
3. One of the basic ways carbon monoxide (CO) causes harm is
a.
b.
c.
d.
it
it
it
it
decreases production of hemoglobin.
produces abnormal hemoglobin.
causes tissue hypoxia.
causes pulmonary or coronary vasoconstriction.
4. Carbon monoxide (CO) can cause
a.
b.
c.
d.
pulmonary capillary vasoconstriction.
production of methemoglobin.
hemolysis.
direct cellular toxicity.
5. Two organs particularly vulnerable to carbon monoxide (CO)
poisoning are
a.
b.
c.
d.
the
the
the
the
brain and the heart.
kidneys and the pancreas.
thyroid gland and the small bowel.
lungs and the liver.
6. True or False: Carboxyhemoglobin (COHb) level is a good
predictor of the seriousness of the carbon monoxide (CO)
exposure.
a. True
b. False
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7. The primary treatment for carbon monoxide (CO) poisoning
in a patient who is conscious is
a.
b.
c.
d.
hydroxocobalamin.
100% oxygen via a facemask.
endotracheal intubation.
methylene blue.
8. Patients who have had carbon monoxide (CO) poisoning are
at risk for
a.
b.
c.
d.
delayed neuropsychiatric sequelae.
increased risk of developing metabolic syndrome.
delayed onset of liver damage.
increased risk of developing Alzheimer’s.
9. True or False: Tobacco combustion produces CO and smokers
have higher COHb levels than non-smokers.
a. True
b. False
10. According to Clardy, et al., which of the following are
indications for the use of HBO?
a.
b.
c.
d.
Age < 5 years or COHb level > 10%
Pregnancy and a COHb >20% or signs of fetal distress
Age > 55 years and headache
Female gender and metabolic acidosis
11. Which of the following are indications for the use of HBO?
a.
b.
c.
d.
The
The
The
The
development
development
development
development
of
of
of
of
delayed myocardial ischemia
shock to the liver
rhabdomyolysis
delayed neuropsychiatric sequelae
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12. The ambient levels of carbon monoxide (CO) in urban areas
have been found to range from 2-40 ppm, but in areas of
heavy automobile traffic the ambient level can reach an
average of
a.
b.
c.
d.
500 ppm.
50 ppm.
100 ppm.
250 ppm.
13. Because of large-scale public education and prevention
programs, carbon monoxide poisoning has become
uncommon in the United States.
a. True
b. False
14. Peak carbon monoxide (CO) levels produced by methylene
chloride inhalation, ingestion, or dermal absorption are
seen
a.
b.
c.
d.
immediately after exposure.
within minutes of exposure.
only if inhaled.
8 hours or longer after exposure.
15. Oxyhemoglobin dissociation indicates the level of
hemoglobin saturation at any level
a.
b.
c.
d.
of lipid peroxidation.
of oxygen tension of the blood.
of cerebral microvasculature.
above toxic levels.
16. The difference between the oxygen level in body tissue and
the oxygen level of hemoglobin
a.
b.
c.
d.
helps drive the transfer of O2 from hemoglobin to tissue.
slows the transfer of O2 from hemoglobin to tissue.
is the primary cause of cellular toxicity.
increases the risk of developing metabolic syndrome.
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17. In carbon monoxide (CO) poisoning the oxyhemoglobin
dissociation curve shifts to the
a.
b.
c.
d.
right and less oxygen reaches the tissues.
left and more oxygen reaches the tissues.
left and less oxygen reaches the tissues.
right and more oxygen reaches the tissues.
18. True or False: In vitro and animal research suggests that
carbon monoxide may have therapeutic value.
a. True
b. False
19. ____________ is an oxygen-transporting and storage
pigment that is found inside cells.
a.
b.
c.
d.
Hydroxocobalamin
Hemoglobin
Myoglobin
Methemoglobin
20. There is evidence that the oxidative stress induced by
_____________ causes neutrophils to adhere to cerebral
microvasculature.
a.
b.
c.
d.
oxygen tension
apoptosis
catecholamine surge
free radicals
21. A patient presents with metabolic acidosis, which is a
symptom of
a.
b.
c.
d.
moderate CO poisoning.
severe CO poisoning.
cyanide poisoning not CO poisoning.
methemoglobinemia
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22. Which of the following conditions is symptomatic of
moderate CO poisoning?
a.
b.
c.
d.
metabolic acidosis
seizures
hypotension
syncope
23. True or False: Levels of COHb that are considered harmless
may cause cognitive impairment.
a. True
b. False
24. Symptoms of delayed neuropsychiatric sequelae (DNS) potential effect of CO poisoning - include affective and
cognitive impairment and the onset of DNS has been
reported to be
a.
b.
c.
d.
within 8 hours of exposure.
more than a year after exposure.
from two days to eight months after exposure.
from 48-72 hours after exposure.
25. The most common side effect of HBO therapy is
a.
b.
c.
d.
lethargy.
syncope.
seizures.
middle ear barotrauma.
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CORRECT ANSWERS:
1. Carbon monoxide (CO) is a gas that is
a. colorless.
“Carbon monoxide (CO) is sometimes called the silent killer,
and aptly so. It is a gas that is produced by incomplete
combustion of carbon-containing material, it is colorless,
odorless, and tasteless, and CO can be lethal.”
2. Carbon monoxide (CO) can be produced by
b. methylene chloride
“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 exposure. Methylene iodide is
used by jewelers to examine gems and, like methylene
chloride, it is converted in vivo to CO.”
3. One of the basic ways carbon monoxide (CO) causes harm is
c. it causes tissue hypoxia.
“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.”
4. Carbon monoxide (CO) can cause
d. direct cellular toxicity.
“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 toxicity, is partially the cause of the
neurologic signs and symptoms of CO poisoning.”
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5. Two organs particularly vulnerable to carbon monoxide (CO)
poisoning are
a. the brain and the heart.
“The signs and symptoms of CO poisoning are vague and nonspecific, but CO is the most toxic to the organs that are the
most metabolically active and have high oxygen demands, so
the brain and the heart are the particularly vulnerable to CO.”
6. True or False: Carboxyhemoglobin (COHb) level is a good
predictor of the seriousness of the carbon monoxide (CO)
exposure.
b. False
“Carboxyhemoglobin levels are also used to determine what
treatment the patient needs 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. The primary treatment for carbon monoxide (CO) poisoning
in a patient who is conscious is
b. 100% oxygen via a facemask.
“Following removal from the source and after a rapid
assessment of the ABCs, oxygen at 100% via a facemask
should be applied; if the patient is comatose, he or she should
be endotracheally intubated. If the patient has chronic
obstructive pulmonary disease and retains carbon dioxide, high
concentrations of oxygen should be used with caution.
Arrhythmias, hypotension, and seizures would be treated with
basic, supportive care.”
8. Patients who have had carbon monoxide (CO) poisoning are
at risk for
a. delayed neuropsychiatric sequelae.
“One potential effect of CO poisoning is delayed
neuropsychiatric sequelae (DNS).”
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9. True or False: Tobacco combustion produces CO and smokers
have higher COHb levels than non-smokers.
a. True
“Tobacco combustion produces CO and smokers have higher
COHb levels than non-smokers.”
10. According to Clardy, et al., which of the following are
indications for the use of HBO?
b. Pregnancy and a COHb >20% or signs of fetal distress
“Recommendations for HBO Therapy by Clardy et al.,…
Pregnancy and a COHb >20% or signs of fetal distress.”
11. Which of the following are indications for the use of HBO?
d. The development of delayed neuropsychiatric sequelae
“Hyperbaric oxygen is routinely used for patients with serious
CO poisoning or patients who do not respond to normo-baric
oxygen therapy and most often, to prevent the development
and/or reduce the severity of DNS. However, important, basic
issues about its use have not been clarified or resolved.”
12. The ambient levels of carbon monoxide (CO) in urban areas
have been found to range from 2-40 ppm, but in areas of
heavy automobile traffic the ambient level can reach an
average of
a. 500 ppm.
“The ambient levels of CO in urban areas have 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.”
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13. Because of large-scale public education and prevention
programs, carbon monoxide poisoning has become
uncommon in the United States.
b. False
“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. Carbon
monoxide poisoning is still very common. Carbon monoxide
poisoning is a leading cause of morbidity and mortality in the
United States.”
14. Peak carbon monoxide (CO) levels produced by methylene
chloride inhalation, ingestion, or dermal absorption are
seen
d. 8 hours or longer after exposure.
“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.”
15. Oxyhemoglobin dissociation indicates the level of
hemoglobin saturation at any level of
b. oxygen tension of the blood.
“The oxyhemoglobin dissociation indicates how saturated
hemoglobin is at any 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.”
16. The difference between the oxygen level in body tissue and
the oxygen level of hemoglobin
a. helps drive the transfer of O2 from hemoglobin to tissue.
“… 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
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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.”
17. In carbon monoxide (CO) poisoning the oxyhemoglobin
dissociation curve shifts to the
c. left and less oxygen reaches the tissues.
“In CO poisoning the oxyhemoglobin dissociation curve shifts
to the left and less oxygen reaches the tissues.”
18. True or False: In vitro and animal research suggests that
carbon monoxide may have therapeutic value.
a. True
“Although the concept is in the experimental stages, in vitro
and animal research suggests that carbon monoxide may have
therapeutic value.”
19. ____________ is an oxygen-transporting and storage
pigment that is found inside cells.
c. 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.”
20. There is evidence that the oxidative stress induced by
_____________ causes neutrophils to adhere to cerebral
microvasculature.
d. free radicals
“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. There is evidence that the oxidative stress
induced by free radicals causes neutrophils to adhere to
cerebral microvasculature.”
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21. A patient presents with metabolic acidosis, which is a
symptom of
b. severe CO poisoning.
“Patients with severe CO poisoning may have arrhythmias,
coma, hypotension, metabolic acidosis, and seizures.”
22. Which of the following conditions is symptomatic of
moderate CO poisoning?
d. syncope
“Patients with mild CO may have confusion, dizziness, fatigue,
headache, nausea, and tachycardia…. Patients with moderate
CO poisoning may have ataxia, chest pain, dyspnea, syncope,
and tachycardia…. Patients with severe CO poisoning may have
arrhythmias, coma, hypotension, metabolic acidosis, and
seizures.”
23. True or False: Levels of COHb that are considered harmless
may cause cognitive impairment.
a. True
“Evidence supporting this is that patients do not always
improve as CO is eliminated; levels of COHb that are
considered harmless may cause cognitive impairment; 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.”
24. Symptoms of delayed neuropsychiatric sequelae (DNS) potential effect of CO poisoning - include affective and
cognitive impairment and the onset of DNS has been
reported to be
c. from two days to eight months after exposure.
“One potential effect of CO poisoning is delayed
neuropsychiatric sequelae (DNS). Symptoms include affective
and cognitive impairment. The onset of DNS has been reported
to be from two days to eight months after exposure. ….
Delayed neuropsychiatric sequelae appear to be relatively
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common, but the exact incidence of this complication is not
known…. The onset of DNS has been reported to be from two
days to eight months after exposure.”
25. The most common side effect of HBO therapy is
d. middle ear barotrauma.
“Most side effects of HBO therapy are mild and temporary.
Middle ear barotrauma such as bleeding, pain, and perforation
of the eardrum is the most common side effect of HBO
therapy.”
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