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Education/Training

Carbon Monoxide Poisoning

Daniel R. Gerard, MS, RN, NRP 

A DC Fire and EMS responder holds a CO detector at a recent call. (Photo: DC Fire and EMS/Twitter)
A DC Fire and EMS responder holds a CO detector at a recent call. (Photo: DC Fire and EMS/Twitter) 

On a brisk winter morning, you’re dispatched for an unknown medical complaint. Upon arrival at the apartment complex, you find a teenage female sitting upright in her living room. She complains of a postsyncopal episode, saying she got out of bed and next remembered waking up on the floor. Her current complaint is abdominal pain. She says she’s on her menstrual cycle and believes that’s the cause.

Her vitals all appear normal. You perform a tilt test, but there are no orthostatic changes. The rest of the physical exam is unremarkable. You transport the patient to the closest ED.

A bit later the attending from the ED calls dispatch and asks to speak with you. You get on the phone, and she tells you the patient had carbon monoxide poisoning. You thank her for the information and immediately contact your on-duty chief, who notifies the fire department.

After evacuation of the building, the fire department and gas company locate the source of the CO: a wall heating unit had a leak. There were also 4 other people in the apartment complex with vague symptoms. They were treated on scene and transported to the ED, where they also had high CO levels upon examination. Thankfully they were treated and released without further negative sequelae.

Epidemiology

Carbon monoxide is a colorless, odorless gas that is highly toxic and can enter a residence through any crevice or opening. It is specifically classified as a hazardous material by the Department of Transportation and listed in the DOT’s Emergency Response Guidebook.

Since it is impossible to see, taste, or smell CO, it may kill victims before they are aware it is in their home. The primary route of exposure is inhalation. The degree of CO poisoning can vary greatly from person to person; age, health status, concentration, and length of exposure all will help determine the outcome of an exposed patient.

In the United States between 170–400 people die every year from CO produced by nonautomotive sources. Examples include faulty furnaces, ranges, water heaters, and room heaters; portable generators; fireplaces; and, believe it or not, charcoal burned in homes and other enclosed areas. Other cases arise from CO produced by cars left running in enclosed spaces.

The Centers for Disease Control and Prevention estimates that several thousand people go to hospital emergency rooms every year for CO poisoning.

Pathophysiology and Assessment

CO has an affinity for binding to hemoglobin molecules that is 250 times greater than oxygen’s. It displaces oxygen from the hemoglobin, preventing it from being carried to tissues. With CO poisoning, CO is carried from the lungs to the tissues instead. This causes a cellular asphyxiation, because the CO molecule is bound so tightly to the hemoglobin molecule, the hemoglobin cannot accept oxygen or carbon dioxide. Since oxygen cannot be delivered to the cells and since CO2 can’t bind to the hemoglobin to be removed, normal oxidative metabolism is inhibited. This causes a buildup of carbon dioxide in the tissues.

As the body becomes hypoxic, minute volume, respiratory rate, and heart rate increase. Since oxygen cannot break the bond between the hemoglobin and carbon monoxide, it becomes a vicious cycle. Myocardial oxygen demand increases, the brain doesn’t get adequate oxygen, and the patient’s heart and respiratory rates continue to increase to compensate. The patient suffers profound mental status changes (confusion, delirium, loss of consciousness), and their vital signs continue to decline.

Without oxygen and with the buildup of carbon dioxide in the vital organs, critical systems fail and die in short order.

Pulse oximeters are unable to distinguish between oxygen and carbon monoxide bound to hemoglobin. SpO2 readings in the presence of carbon monoxide will be falsely elevated. Do not use pulse oximetry to screen patients in suspected cases of carbon monoxide exposure. A “normal” pulse oximetry reading in this scenario never means a patient is oxygenated adequately. A full-panel arterial blood gas reading that includes carboxyhemoglobin should be obtained in the ED.

The latest tool in assessment is the fingertip pulse CO-oximeter/light wavelength monitor to detect carboxyhemoglobin in the patient’s blood. It is a noninvasive device that provides continuous measurement of the patient’s carboxyhemoglobin.

Signs and Symptoms

The initial presentation of CO poisoning may be nonspecific, with variable signs and symptoms. Commonly patients will present with headache, dizziness, weakness, nausea, vomiting, chest pain, and altered mental status. This presentation has often been confused with flu, fatigue, and myocardial infarction.

The symptoms of severe CO poisoning include:

  • Malaise
  • Shortness of breath
  • Headache
  • Nausea
  • Chest pain/angina
  • Irritability
  • Ataxia
  • Altered mental status/impaired memory
  • Syncope
  • Loss of consciousness
  • Coma
  • Death

Other signs of carbon monoxide poisoning include:

  • Tachycardia
  • Tachypnea
  • Hypotension
  • Arrhythmias
  • Depressed S-T segment on the electrocardiogram
  • Myocardial ischemia or infarction
  • Noncardiogenic pulmonary edema
  • Cyanosis

Cherry-red skin, once believed to be a hallmark sign of CO poisoning, is actually a late sign and generally noticed on autopsy. It is rarely seen in patients who are alive. If looking for cherry-red presentation, examine the conjunctiva of the eye and oral mucosa first. The absence of cherry-red skin should not eliminate the suspicion of carbon monoxide poisoning.

Patients who tell you their symptoms resolve if they go outside but return once they come back should alert you to possible CO poisoning. Other red flags include flu symptoms without fever, history of exposure, and multiple patients at the same scene with similar complaints.

Treatment

Evacuate the premises, regardless of whether people have specific medical complaints. Every patient is different, and some may tolerate higher levels of carbon monoxide with few or no symptoms. Conversely, patients with cardiac, respiratory, or diabetic histories may be susceptible to extremely low levels of CO. Their presenting conditions will be worse compared to other patients with similar exposures.

Decontamination for inhalation exposure is respiratory. Remove the patient from the source. This is critical for any exposure where inhalation is the primary source. Place them on 100% O2 as soon as possible. The half-life for carbon monoxide is 5–9 hours on room air and 60–90 minutes on 100% oxygen.

Treat underlying conditions. If the patient is wheezing, institute your asthma protocol. If they complain of chest pain, perform a 12-lead EKG and treat per protocol. If they’re hypotensive, start an IV and infuse normal saline. A caveat: Carbon monoxide is an asphyxiant, and it may precipitate a cardiac or respiratory event.

Monitor IV access, cardiac readings, SpCO, and SpO2. SpO2 in the carbon monoxide-exposed patient should be normal and may even be elevated. If the SpO2 drops, it may point to another underlying problem.

If the patient is symptomatic and has been exposed to carbon monoxide, regardless of the reading on the fingertip pulse CO-oximeter/light wavelength monitor, they must be transported and evaluated for CO poisoning.

Treatment at the hospital will be driven by several factors. After obtaining blood gases to confirm if the patient has elevated carboxyhemoglobin, the care team may, if warranted, send the patient directly to a hyberbaric chamber for treatment.

Treatment with hyberbaric oxygen will reduce the half-life of carbon monoxide to 20 minutes. Pregnant patients and those with existing cardiac or respiratory disease may be sent directly to the hyperbaric chamber even with relatively low levels of CO detected in the blood.

Patients are treated symptomatically, but even with prompt, efficient treatment, the neuropsychiatric effects of carbon monoxide poisoning are difficult to predict. Some patients may develop long-term brain damage.

Summary

Carbon monoxide poisoning is not your typical EMS/hazmat response. It represents several challenges to scene management, assessment, and appropriate treatment. The fingertip pulse CO-oximeter offers a new dynamic to triage and assessment. Development of appropriate protocols will dictate response, clinical care, and operations, all essential to success in responding to these types of incidents.

Resources

Agency for Toxic Substances and Disease Registry. Carbon Monoxide. Accessed July 20, 2022. wwwn.cdc.gov/TSP/substances/ToxSubstance.aspx?toxid=253

Agency for Toxic Substances and Disease Registry. Managing Hazardous Material Incidents. Published March 2011. Accessed July 20, 2022. www.atsdr.cdc.gov/mhmi/index.html

Centers for Disease Control and Prevention. Clinical Guidance for Carbon Monoxide (CO) Poisoning. Accessed July 20, 2022. www.cdc.gov/disasters/co_guidance.html

Hardy KR, Thom SR. Pathophysiology and treatment of carbon monoxide poisoning. J Toxicol Clin Toxicol. 1994; 32(6): 613–29. doi: 10.3109/15563659409017973

Hnatov MV. Non-Fire Carbon Monoxide Deaths Associated with the Use of Consumer Products. Consumer Product Safety Commission. Published December 2018.

National Institute for Occupational Safety and Health. Carbon monoxide. Accessed July 20, 2022. www.cdc.gov/niosh/npg/npgd0105.html

Daniel R. Gerard, MS, RN, NRP, is president of the International Association of EMS Chiefs. He is a recognized expert in EMS system delivery and design, EMS/health-service integration, and service delivery models for out-of-hospital care.

 

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