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S35 Simple and Chemical Asphyxiants

Asphyxiants: Simple and Chemical

Ken-Hing Tan, MD; Tzong-Luen Wang, MD, PhD

Asphyxiants are gases that cause tissue hypoxia. They are classified as either simple or chemical on
the basis of the mechanism of toxicity. Simple asphyxiants decrease FiO2 by displacing oxygen in
inspired air, results in hypoxemia. Chemical asphyxiants interfere with oxygen transport system and
cellular respiration and thereby cause tissue hypoxia. Mild symptoms of asphyxia include headache,
dizziness, nausea, and vomiting. More severe symptoms range from dyspnea, altered sensorium,
cardiac dysrhythmia, ischemia, syncope, seizure, and even death. Clinical diagnosis of asphyxiant
exposure is limited. A consistent history, myriad spectrum of complaints, group victims, and rapid
resolution on away from exposure are generally sufficient. Occupational exposures and fires are the
most common sources of inhalation injuries. Working in confined spaces are harzardous to workers.
Rapid removal, supportive care and preventing hypoxemia are the mainstay of treatment. Emer-
gency planning should be applicable to both accidental and deliberate chemical disasters. (Ann
Disaster Med. 2005;4 Suppl 1:S35-S40)

Key words: Asphyxiants; Asphyxiation; Toxic Inhalation; Carbon Monoxide; Cyanide; Hydro-
gen Sulfide

Introduction hypoxemia, secondary to gases inhalation.4

Asphyxiants are gases that deprive body tissues Occupational exposures and fires are the most
of oxygen. They are generally divided into two common sources of the numerous agents ac-
categories, simple and chemical. 1 Simple countable for accidental inhalation injuries.When
asphyxiants merely displace oxygen from ambi- obvious historical evidence or a heightened sus-
ent air whereas chemical asphyxiants react in the picion for an acute inhalation exposure does not
human body to interrupt either the delivery or exist, misdiagnosis and maltreatment are likely
utilization of oxygen.2 When the concentration to occur.
of any gases increase, the fraction of inspired Clinical diagnosis of simple asphyxiant ex-
oxygen (FiO2) tends to decrease, rendering to posure is limited. A consistent history, myriad
hypoxemia. spectrum of complaints, group of victims, and
Working in confined spaces are hazard- rapid resolution on away from exposure are
ous to workers.3 The death is usually due to generally sufficient. Identification of particular

From Department of Emergency Medicine, Shin Kong Wu Ho-Su Memorial Hospital, Taipei, Taiwan; Medical College, Taipei
Medical University, Taipei, Taiwan
Address for reprints: Dr. Tzong-Luen Wang, Department of Emergency Medicine, Shin-Kong Wu Ho-Su Memorial Hospital, 95
Wen Chang Road, Taipei, Taiwan
Received: Sep 5 2005. Revised: Sep 13 2005. Accepted: Sep 20 2005.
TEL: 886-2-28389425 FAX: 886-2-28353547 E-mail:

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Simple and Chemical Asphyxiants S36

gases is not necessary except for government Many cases of CO poisoning, even re-
health politics. cover well without any complication with hy-
Supportive care and preventing hypoxemia perbaric or high oxygen therapy, revisit hospi-
is central to the treatment of all pulmonary and tal with delayed neuropsychiatry sequelae, such
systemic inhalation injuries.5 Patients at risk for as cognitive and personality changes,
hypoxia should be observed for the delayed incontinence, dementia, and psychosis.8
development or progression of post hypoxic
neurological sequelae. Clinical Features
Decrease FiO2 from ambient, (i.e., 21%) to
Classification 15% brings acute effects of hypoxia within min-
Simple asphyxiants, such as carbon dioxide utes after exposure to simple asphyxiant. It re-
(CO2), Nitrogen (N2), and Propane (C3H8), sults in autonomic stimulation (e.g., tachycardia,
when present in high concentrations in air, es- tachypnea, and dyspnea) and cerebral hypoxia
pecially within a confined space, act by limiting (e.g., ataxia, dizziness, incoordination, and
the utilization of the oxygen, without producing confusion). Life probably cannot be sustained
significant toxic effects on the body per se. at a FiO2 level below 6%.9
Clinical reports on unintentional mass ex-
posure to extreme concentrations of carbon Carbon Dioxide
dioxide occurs in Israel, caused by a leakage Carbon dioxide (CO2) is a colorless, odorless,
of container of liquid carbon dioxide in an en- nonirritating gas that is widely used as a fire
closed working environment. Twenty-five ca- extinguisher, in ice-making factories and oc-
sualties developed symptoms included dyspnea, cupational or recreational (diving) settings. The
cough, dizziness, chest pain, and headache. It potential severity of toxicity from carbon diox-
resulted in significant but transient cardiopulmo- ide was tragically exemplified by the disaster in
nary morbidity with no mortality when victims Cameroon in 1986, when many people were
were promptly evacuated and given supportive killed by the expulsion of carbon dioxide from
therapy.6 a volcano.11
Most diving injuries are related not only CO2 closely resembles simple asphyxiants
to barotraumas, decompression illness, pulmo- from a toxicological standpoint. CO2 in high
nary edema, but also nitrogen narcosis at el- concentration, however, has direct toxic
evated levels. 7 effects, mainly those of sympathetic
Another categories of asphyxiants, i.e., stimulation, including increased heart rates,
chemical such as carbon monoxide (CO), cya- cardiac output, mean pulmonary artery
nide (CN-), and hydrogen sulfide (H2S), bind pressure, and pulmonary vascular resistance, and
to and inhibit the ultimate step in electron trans- therefore impose excess load on the
port chain system of the mitochondria, the Fe3+ myocardium. The most important action in CO2
containing cytochrome a-a3 in complex IV, intoxication is to remove the victims from the
therefore, rendering tissue hypoxia and the de- exposed environment and to provide cardio-
velopment of lactic acidosis. respiratory support until spontaneous recov-

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S37 Simple and Chemical Asphyxiants

ery occurs.6 discharges.

The key to the pathogenicity of CO is its
Nitrogen propensity to attach itself to the ferrous (Fe3+)
Nitrogen gas (N2) is a colorless, odorless, in the heme prosthetic group of hemoproteins,
tasteless, and constitutes about 80% of air in which includes hemoglobin, myoglobin, and
atmosphere. The incident rate of nitrogen nar- some intracellular enzymes (cytochromes, P-
cosis (12%) is the most frequent, followed by 450). Contributing to tissue hypoxia is the fail-
barotraumas of the ear (11%) and paranasal si- ure of carboxyhemoglobin to dissociate in the
nus (5.6%) during scuba diving. 11 The major tissues.15
toxic effect is simple asphyxiation. N2 is thought Mild CO poisoning occurs frequently,
to act by interacting directly with neuronal ion- leading to headache, nausea, vomiting, dizziness,
channel receptors i.e., [gamma] - aminobutyric myalgia or confusion. However, in severe CO
acid (GABA) receptor antagonists.12 intoxication, patients suffered from neuropsy-
chiatry abnormality or cardiovascular instability
Propane (e.g. alter sensorium, seizure, coma, syncope,
Propane (C3H8), which is both colorless and ischemia, infarction, or dysrthymia). It would
odorless in its gaseous state, has highly flam- depress myocardium contractility and lead to
mable and explosive characteristics. It displaces acute rhabdomyosis.
oxygen, consequently causing hypoxia and
eventually anoxia. The depletion of oxygen in Hydrogen Cyanide
the air, and the build up of propane and carbon Cyanides (CN-) are utilized in mining operations,
dioxide, lead to unconsciousness and eventual photographic materials, the production of
death. Death results not from the toxic nature plastics, pigments, and dyes, and often used as
of the gas but simply from the displacement of fumigant pesticides.During fires, victims can also
atmospheric oxygen.13 inhale significant carbon monoxide and cyanide
Inhalation of gaseous propane can cause gases, which may cause synergistic toxicity in
dizziness, nausea, vomiting, confusion, humans.
hallucinations, and a feeling of euphoria. At high CN- is described as a cellular toxin be-
concentrations, it has a narcotic effect and can cause it inhibits aerobic metabolism. It revers-
bring about cardiac arrest resulting from sup- ibly binds to cytochrome oxidase and inhibits
pression of central nervous system activity.14 the last step of mitochondrial oxidative
phosphorylation. This inhibition halts carbohy-
Carbon monoxide drate metabolism from the citric acid cycle, and
Carbon monoxide (CO) is, after carbon intracellular concentrations of adenosine triph-
dioxide, the most abundant atmospheric osphate are rapidly depleted. 16
pollutant. It originates partly from natural sources With the inhalation of high concentration
such as forest fires and volcanic eruptions, but hydrogen cyanide (300 mg/m3), the victim’s skin
mostly from human activity, in particular from is a flushed reddish pink, and tachypnea,
the internal combustion engine and industrial tachycardia, and nonspecific central nervous

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Simple and Chemical Asphyxiants S38

symptoms appear. Stupor, coma, and seizure presentations. The circumstances and locations
immediately precede respiratory arrest and car- of the exposure, presence of combustion or
diovascular collapse. Death shortly occurs. odors, and number and condition of victims as-
sist in diagnosis.
Hydrogen Sulfide In case of chemical asphyxiant, there are
Hydrogen sulfide (H2S) is a colorless, flammable certain kinds of laboratory test (CO-oximeter,
gas. H2S has a pungent odor reminiscent of rot- pulse oxymetry, arterial blood gas, MetHb level,
ten eggs. There is the potential for widespread lactate) can be used to aid in confirm diagnosis.
occupational exposure to H2S, including in the
oil and water treatment industries. H2S selec- Treatment
tively binds to the enzymes involved in cellular Rapid removal, away from the asphyxiant, and
respiration thereby causing a shift towards supportive treatment with oxygen supplement
anaerobic respiration. are the mainstay of treatment. Neurological in-
At higher concentrations, death is caused jury and cardiorespiratory instablability should
by depression of respiratory center in the brain; be managed with standard resuscitation
at lower concentrations, death is caused by protocols.
pulmonary edema and congestion. Survivors Patients with asymptomatic or mild poi-
wtih periods of unconsciousness may suffer soning who recover after removal from the ex-
permanent neurological sequelae such as posure can be observed briefly and referred to
memory loss. High exposures to near lethal con- outpatient for follow up of possible delayed
centrations in animals have shown destruction neurological sequalae. Patients who are at risk
to nasal epithelium. During vigorous exercise, of hypoxia, such as cardiopulmonary co-
low level exposures (5–10 ppm) cause a shift morbidity, advanced age, or exacerbating medi-
to anaerobic respiration, leading to increased cal conditions, should admitted for further man-
lactic acid formation. Eye irritation, so-called agement and observation.
“gas eye, only occurs at high exposure In cases of carbon monoxide, cyanide or
concentrations.17 hydrogen sulfide, administer 100% oxygen.
Oxygen reverses hypoxemia and accelerates the
Diagnostic Strategies elimination of asphyxiants. 19 HBO has been
Clinical diagnosis of simple asphyxiant exposure shown to be the standard treatment for severe
is limited. A consistent history, myriad spectrum CO poisoning. It reverses hypoxia, competes
of complaints, group of victims, and rapid reso- with CO for hemoglobin binding, and promotes
lution on away from exposure alert the suspi- carboxyhemoglobin dissociation. It shortens
cion of asphyxic agent. The diagnosis always carboxyhemoglobin half-life from 4–6 h to <30
required scene investigation by a trained and min.20
outfitted team. CN- poisoning is treated with amyl nitrites,
Since the presenting complaints are non- sodium nitrite and thiosulfate, all of which are in
specific and protean, alertness should be kept the Antidote Kit. Nitrite induces the formation
for those who visit ED with unusual of methemoglobin, which is bound by CN-,

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S39 Simple and Chemical Asphyxiants

yielding cyanomethemoglobin. Thiosulfate acts acute inhalation exposure does not exist, mis-
synergistically to accelerate the detoxification diagnosis and maltreatment are likely to occur.
of CN- to thiocyanate.21, 22 Supportive care and preventing hypoxemia is
For CN - poisoning due to smoke central to the treatment of inhalation injuries.
inhalation, most authorities recommend the use Antidotes and hyperbaric therapy aid in treat-
of thiosulfate, oxygen, and supportive measures. ment of specific chemical asphyxiant. Patients
Nitrite-induced methemoglobinemia aggravates at risk for hypoxia should be observed for the
the decrease in oxygen-carrying capacity that is delayed development or progression of post
due to carboxyhemoglobinemia. 23 hypoxic neurological sequelae.Alertness should
The treatment of victims of H2S poisoning be paid on group of victims who visit ED with
is similar to that used for hydrogen cyanide unusual presentations of illnesses.
poisoning. It involves parenteral administration
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