CARBON MONOXIDE POISONING

Author: Mark Goldstein, RN, BSN, EMT-P I/C, Royal Oak, Mich

Earn Up to 8.5 CE Hours. See page 592.

Carbon monoxide is a colorless, odorless, tasteless,nonirritating gas and an old enemy to human health.Carbon monoxide poisoning is a rare illness, which is

sometimes hard to differentiate and diagnose. Emergencynurses need to be aware of this illness and how to diagnoseand treat it, as it is one of the most infamous poisons thatsilently takes many lives. Carbon monoxide was the leadingcause of poisoning death in the United States from 1979 to1988 according to a death certificate review (>5,000 deathsper year).1 According to the Centers for Disease Controland Prevention and the 2005 National Health Care Survey,there were over 500 unintentional deaths and greater than2,000 suicides that were a direct result of carbon monoxidepoisoning.2 Half of the unintentional (non-fire) poisoningswere from automobile exhaust; however, smoke inhalationis estimated to be the greatest cause of accidental exposure.

Annually, there are over 40,000 ED visits that are re-lated to carbon monoxide poisoning.3 These ED visits areusually in a northern climate and during the winter season. Itis estimated that more than 10,000 people lose at least 1 dayof work each year because of carbon monoxide exposure.4

According to annual statistics compiled by the NationalFire Protection Association, smoke inhalation and carbonmonoxide poisoning are consistently a common source offire-related death and injury.5 There are delayed conse-quences to exposure, which result in neurologic sequelaeand are almost certainly underestimated as a result of thenumber of fire deaths that do not include carbon monoxideas a cause of death.6 The final result is an estimated case fatal-ity rate of 0% to 31%. Carbon monoxide remains a healthconcern despite the various educational and technologic ad-vancements with regard to its negative human effects.7

Causes of Carbon Monoxide Poisoning

Carbon monoxide comes from both natural and manufac-tured sources. The largest risk of exposure comes from the

household environment.8 Such exposures come from theinhalation of combustible fumes such as those producedby small gasoline engines, stoves, generators, lanterns,and gas ranges or by burning charcoal and wood. Carbonmonoxide is usually inhaled from an enclosed or confinedspace such as a garage, kitchen, basement, or workroom.The fire-related injuries and deaths result from a mixtureof small particles of asphyxiant and irritant gases fromthe chemical breakdown of its burned sources such asfurniture or other household items.9 Acute exposure fromcarbon monoxide poisoning can come from any fossilfuel.10 Chronic carbon monoxide exposure can come fromtobacco smoke, automotive exhaust (truck drivers stuck intraffic), and occupational or industrial sources (steel found-ries, paper mills, methylene chloride).11

Carbon monoxide detectors have helped reduce theincidence and prevalence of unintentional exposures.12

The increasing popularity of carbon monoxide detectorshas grown throughout the years through education andprevention measures. However, despite the increased use ofthese detectors, not everyone is familiar with carbon mon-oxide health risks in the home.13 Carbon monoxide can killwithin seconds to hours depending on the dose. A patient canbe exposed to a small amount of carbon monoxide over along period of time or to a large amount of carbon monoxideover a short period of time, with toxic levels developing.14

The concentration of carbon monoxide is measured in partsper millions and is the determining factor in symptoms. Ac-cording to the US Department of Labor, a healthy patientcan be exposed to a carbon monoxide concentration as lowas 35 ppm for up to 8 hours with no adverse effects.15 Listedin Table 1 are the concentrations of carbon monoxide andthe associated symptoms. There is a ceiling limit of 200 ppm(measured over a 15-minute period).

Mechanisms of Carbon Monoxide Poisoning

The best established and most important toxic action of car-bon monoxide is incapacitation of the cell’s mechanism forusing oxygen resulting in chemical asphyxiation and hypoxia(e.g., effective oxygen deprivation). Hypoxia is a deficiency ofoxygen at the tissue level.16 Hypoxemia-induced hypoxia oc-curs when the oxygen tension of arterial blood is reduced—generally, a partial pressure of oxygen (Po2) of less than80mmHg.17 Carbonmonoxide prevents cells from using oxy-gen by inhibiting the quadri-helical receptive function of thecarboxyhemoglobin (COHb) molecule in the red blood cell.

Mark Goldstein, Michigan ENA, is EMS Coordinator, Department of Emer-gency Medicine, William Beaumont Hospital, Royal Oak, Mich.

For correspondence, write: Mark Goldstein, Department of Emergency Medi-cine, William Beaumont Hospital, 3601 Thirteen Mile Rd, Royal Oak, MI48073; E-mail: mgoldstein@beaumonthospitals.com.

J Emerg Nurs 2008;34:538-42.

Available online 27 June 2008.

0099-1767/$34.00

Copyright © 2008 by the Emergency Nurses Association.

doi: 10.1016/j.jen.2007.11.014

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As COHb decreases the available oxygen binding sites,less total oxygen is being carried and there is a downwardshift in the oxygen dissociation curve.18 Because there is anincrease in the hemoglobin’s affinity for oxygen, particu-larly at low Po2 levels, such as in tissue, hemoglobin can-not release its bound oxygen at the tissue level. This shiftsthe oxygen dissociation curve left and into an asymptoticshape (Figure).

Hemoglobin is a tetramer with 4 oxygen binding sites.The affinity for carbon monoxide to the site of the tetra-mer receptor site is 200 times greater than the oxygen mole-cule.19 Oxygen molecules normally bind to the receptor siteswithin the red blood cell and are transported throughout thebody for use. Carbon monoxide, which has a chemical struc-ture similar to oxygen, also binds to the red blood cell. Thebinding of carbon monoxide competitively inhibits the abilityof the red blood cell to bind with oxygen and thereby reducesthe transport of oxygen, which results in histotoxic hypoxia.

Manifestations of Carbon Monoxide Poisoning

The body relies on oxygen to reach the cells to function;therefore all body systems are affected by carbon monoxidepoisoning. The heart, brain, and lungs require large con-tinuous amounts of oxygen for normal function and are mostsusceptible to the effects of carbon monoxide poisoning.Early signs and symptoms reflect reflexive attempts of therespiratory, cardiovascular, and neurologic systems to over-come tissue hypoxia. Carbon monoxide poisoning oftenmimics a viral illness with flu-like symptoms such as fatigue,lethargy, somnolence, malaise, nausea, vomiting, and dizzi-ness.20 Of the flu-like symptoms, the most common areheadache, nausea, and dizziness.

Carbon monoxide also binds to cardiac myoglobin,which means there are less oxygen molecules for aerobicmetabolism. This results in decreased cardiac contractilityand decreases oxygen delivery evenmore (low-flow hypoxia).There are other clinical effects that are due to widespreadischemia, including rhabdomyolysis, pulmonary edema,multiorgan failure, disseminated intravascular coagulation,dermal injury, and renal failure.21 Carbon monoxide expo-sure can also be made worse by comorbidities such as con-gestive heart failure, anemia, drug ingestion, burns, trauma,and smoke inhalation.22 Degrees of exposure with relationto toxicity and severity are affected by relative amounts ofcarbon monoxide, oxygen, actual exposure, and ventilationminute volume.

Recognition of Carbon Monoxide Poisoning

Carbon monoxide remains a challenge to detect becauseof the chemical properties of being a colorless, odorless,tasteless, nonirritating gas. Acute carbon monoxide poison-ing should be suspected in anyone who inhales smoke ina closed-space fire. The clinical manifestation and diag-nostic findings in carbon monoxide poisoning reflect hyp-oxia caused by carbon monoxide deactivation of cellularoxygen-utilization mechanisms. The development of toxicityis generally rapid, at a rate dependent on the amount of expo-sure. Exposure to large doses of carbon monoxide producesmarked symptoms nearly immediately and can result in deathwithin minutes.23 Onsets of symptoms from chronic expo-sures from smoking, automobiles, and occupational or indus-trial sources have been reported to take up to 2 to 3 years.24

There are no reported controlled clinical trials of chroniclow-level exposures.

TABLE 1Carbon monoxide concentrations, COHb levels, and associated symptoms

Carbon monoxide concentration COHb level Signs and symptoms

35 ppm <10% Headache and dizziness within 6 to 8 h of constant exposure100 ppm >10% Slight headache in 2 to 3 h200 ppm 20% Slight headache within 2 to 3 h; loss of judgment400 ppm 25% Frontal headache within 1 to 2 h800 ppm 30% Dizziness, nausea, and convulsions within 45 min; insensible within 2 h1,600 ppm 40% Headache, tachycardia, dizziness, and nausea within 20 min; death in

less than 2 h3,200 ppm 50% Headache, dizziness, and nausea in 5 to 10 min; death within 30 min6,400 ppm 60% Headache and dizziness in 1 to 2 min; convulsions, respiratory arrest,

and death in less than 20 min12,800 ppm >70% Death in less than 3 min

Data from Struttmann T, Scheerer A, Prince S, Goldstein L. Unintentional carbon monoxide poisoning from an unlikely source. J Am Board Fam Pract 1998;11:481-4.

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The clinical presentation of acute carbon monoxidepoisoning can change rapidly. Health care providers usuallyfirst encounter patients after moderate to severe toxicity hasdeveloped. Increases in blood pressure, heart rate, and re-spiratory rate, as well as chest pain, shortness of breath,impaired judgment, dizziness, anxiousness, nausea, andheadache, are common early signs and symptoms.25 Latesigns and symptoms of carbon monoxide poisoning arecherry-red skin, hypotension, poor capillary refill, uncon-sciousness, seizures, coma, and cardiac arrest.

Hallmark laboratory findings in acute carbon monox-ide poisoning come from COHb levels, measurements ofvenous blood gases, complete blood count assessment, lac-tate levels, and cardiac enzyme levels, including myoglobin.26

COHb is formed by the union of carbon monoxide andhemoglobin and is a marker of carbon monoxide poison-ing. COHb concentrations of normal healthy individualsare less than 3%. Individuals who are smokers have COHblevels of up to 9%.27 Carbon monoxide toxicity correlateswith COHb levels (Table 2). Dangerous levels of carbonmonoxide exposure with relation to COHb are levels greaterthan 25%, and levels greater than 50% may result in death.However, there is no direct relationship of clinical effectsand response with COHb levels.28 Therefore COHb levelsare estimates and a guide to help determine exposure levels.

Additional important laboratory values are arterial bloodgases and venous blood gases. Specific values within the

gases measured are the Po2 levels. Normal arterial Po2 levelsare 80 to 100 mm Hg and venous Po2 levels are around25 mm Hg for healthy nonsmokers. Arterial blood gas re-sults will typically be normal or low, and they measure dis-solved oxygen and not bound oxygen. In contrast, venousblood gas Po2 results will usually be high. Venous Po2 levelsaround 30 to 50 mm Hg indicate significant carbon mon-oxide exposure and poisoning.

Treatment of Carbon Monoxide Poisoning

Acute carbon monoxide poisoning is treated by terminatingexposure and administering supportive care.29 Termina-tion of carbon monoxide exposure can entail removal ofthe patient from the exposed environment. Immediate ini-tial emergency care involves the basic life support airway,breathing, and circulation process.30 Administration of15 L/min of oxygen via a non-rebreather mask (NRB) isan integral part of the initial management of acute carbonmonoxide poisoning. High-flow oxygen by an NRB re-duces the half-life of COHb from 300 minutes to 90 min-utes in isobaric conditions. Treatment of mild symptoms ofcarbon monoxide poisoning includes 15 L/min of oxygenvia an NRB for 4 hours with periodic reassessments.31 Ifthere is no improvement after 4 hours and other causeshave been ruled out, one should consider the need for fur-ther treatment.

Treatment for moderate to severe symptoms includeshigh-flow oxygen via an NRB, possible intubation, admis-sion to the intensive care unit for cardiac monitoring, car-diovascular and respiratory support, subsequent neurologicevaluation, and if available, hyperbaric chamber oxygena-tion (HBO) therapy.32 The treatment of HBO reducesthe half-life of COHb to 30 minutes. HBO therapy alsoincreases the amount of oxygen dissolved in the blood from0.3 mL/dL with isobaric oxygen therapy (fraction of in-spired oxygen, 100%) to 6 mL/dL.

There are no absolutes in terms of laboratory values.33

Critically ill patients such as those who are in shock or areunconscious should be fully resuscitated. Where available,treatment of moderate to severe carbon monoxide expo-sure may be enhanced by HBO therapy.34 Indicationsfor definite HBO therapy include altered mental status,abnormal neurologic examination, loss of consciousnessor syncope, seizure, hypotension, myocardial ischemia, ex-treme exposures, and pregnancy with a COHb level greaterthan 15%. Relative indications for HBO therapy may in-clude persistent neurologic symptoms (e.g., headaches ordizziness) after 4 hours of high-flow oxygen therapy viaan NRB, persistent acidosis, concurrent thermal or chemi-cal burns, and pregnancy with a history of any carbon mon-oxide exposure.35

F I G U R E

Oxygen dissociation curve of blood oxygen and oxygen partial pressure.Reprinted with permission from Jain KK. Carbon monoxide poisoning. St.Louis: Warren Green, Inc.; 1990. This figure is available in color and as afull-page document at www.jenonline.org.

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Intentional and incidental carbon monoxide poisoningis a rising concern.36 Considerations of incidental carbonmonoxide poisoning in which the story does not add upmay require involvement of psychiatric and social services.Health care providers may need to notify police and firedepartments of the possibility of more victims. A large pro-portion of carbon monoxide poisonings are intentional.

Special Consideration (Pregnancy)

Pregnancy and carbon monoxide exposure does not in-crease the maternal risk of carbon monoxide toxicity.37

However, the fetus is susceptible to the toxic effects ofmaternal hypoxia.38 Fetal hemoglobin has an even greateraffinity than adult hemoglobin for carbon monoxide bind-ing.39 COHb levels above 15% represent severe poisoning.Therefore recommendations for treatment with HBO ther-apy for pregnant patients should be considered early on.

Injury Prevention Education

Injury prevention and education are the key to awareness ofcarbon monoxide exposure and poisonings.40 Fire depart-ments, EMS providers, public health departments, andhospitals have provided sundry opportunities for publicawareness and education. Despite substantial educationalefforts, carbon monoxide exposures and poisonings stillare an important topic of discussion. Injury prevention ac-tivities, such as lowering the cost of carbon monoxide andsmoke detectors for purchase at a commercial cost, havehelped. Safety fairs and fire department annual open housesoffer free detectors. These life-saving detectors should in-clude semiannual inspection to include providing a newbattery. In most incidents in which a detector was present,a nonworking battery was noted.

Education should include the following recommen-dations: use fuel-burning appliances only if they have beeninstalled by a qualified technician; have fireplaces and chim-neys inspected regularly to ensure proper ventilation; do not

use gas or charcoal barbecue grills indoors or burn charcoalin a fireplace; do not start a car or gas-powered tools such asa lawnmower or snow blower in a closed garage; do not rungas-powered generators in an enclosed garage or basement;replace unvented space heaters with vented space heaters;and do not use gas ovens for heating purposes.

Conclusion

Acute carbon monoxide poisoning can be challenging todiagnose even for the seasoned emergency nurse. It can alsobe a debilitating and sometimes lethal illness if not recog-nized immediately. Therefore emergency nurses shouldhave a comprehensive understanding with regard to recog-nition and treatment of carbon monoxide poisoning. Car-bon monoxide affects all body systems, and progressionand severity of toxicity vary according to concentration andduration of exposure. Morbidity and death are preventableif appropriate intervention is administered in a timely man-ner. Treatment starts with basic life support and oxygen ther-apy. Moderate to severe cases may include advanced airwaytechniques and HBO therapy. Most importantly, injury pre-vention and education are a vital part of reducing the inci-dence and prevalence of exposure and poisoning. This canbe performed by obtaining a carbon monoxide detector andensuring that it is functioning with frequent evaluations.

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TABLE 2Signs and symptoms correlated with COHb level toxicity

Mild poisoning Moderate poisoning Severe poisoning

COHb level <30% and patienthas no signs or symptoms

COHb level between 30% and 40%and patient may or may not have symptoms

COHb level >40% and patienthas symptoms

Headache, nausea, dizziness,fatigue, somnolence, malaise,chest pain nausea, and vomiting

Headache, nausea, dizziness, fatigue,somnolence, malaise, chest pain nausea,and vomiting

Cherry-red skin, lethargy, hypotension,poor capillary refill, unconsciousness,syncope, seizures, coma, andcardiac arrest

Reprinted from Guest HB. Symptoms associated with a given concentration of CO over time. Frequently asked questions about carbon monoxide detectors. Available at:http://www.carbonmonoxidekills.org.uk/linkstore/Carbon%20Monoxide%20Frequently%20Asked%20Questions.htm. Accessed March 14, 2007.

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