The Heart Dangers of CO

Understanding cardiovascular risks to responders from CO exposure



Bryan E. Bledsoe, DO, FACEP | | Wednesday, January 21, 2009

Carbon monoxide (CO) poisoning isn't as simple a process as was once thought. Although we've long known of the short-term effects of CO poisoning, we haven't really understood its long-term effects. A growing body of scientific literature clearly demonstrates that CO exposures, both acute and chronic, can result in long-term complications, including neurological diseases, cardiovascular diseases and similar problems. Further, CO exposure may play a role in firefighter deaths that have been previously ascribed to cardiovascular disease.

It's a well-known fact that nearly half of on-duty, fire-related deaths are due to cardiovascular disease.(1,2) Generally, these deaths have been attributed to coronary artery disease. A recent study found that most on-duty fire-related deaths occur during active fire suppression activities (seeFigure 1:Deaths from Coronary Heart Disease Based on Duty Type). However, firefighter deaths were reported during all aspects of duties, including 9% related to EMS and non-fire emergencies.(3)

Studies suggest that many of these cardiovascular deaths are due to a lack of physical fitness, obesity and similar risk factors.(4,5) Although it seems intuitive that cardiovascular risks in first responders should be similar to those of the population as a whole, other factors must be considered. CO exposure is an occupational hazard of firefighting. In addition, we know that most CO-related deaths result from ventricular fibrillation. However, many fire scenes aren't staffed by EMS personnel, and automated external defibrillators (AEDs) aren't always available. Because of this, the recent National Fire Protection Association (NFPA) Guideline 1584Standard on the Rehabilitation Process for Members During Emergency Operations and TrainingExercises, soon to take effect, mandates the presence of medical personnel on the fireground.

As EMS providers responding to high CO environments to deliver rehab and patient care services, you should be aware of these dangers, as well as precautions you can take to minimize your risk.

Understanding CO

Carbon monoxide is the most common cause of poisoning in industrialized countries. Although French physician Claude Bernard first described CO in 1857, the pathophysiology of CO poisoning is quite complex, and the full effects of exposure are still not fully understood.(6)

Primarily, CO competes with oxygen for oxygen-binding sites on hemoglobin. But CO has a much greater affinity (approximately 200Ï250 times) for these binding sites than oxygen. Thus, CO will quickly bind to available oxygen-binding sites and also displace previously bound oxygen. The binding of CO to hemoglobin results in the formation of a compound called ˙carboxyhemoglobinÓ (COHb).

COHb doesn't transport oxygen. As COHb levels rise, the oxygen-carrying capacity of the blood decreases. The inadequate oxygen delivery to essential tissues results in limited energy production and the production of dangerous chemical by-products, such as lactic acid. Tissues with the highest oxygen demandsƒprimarily in the nervous and cardiovascular systemsƒare most vulnerable to the effects of CO.

Following CO exposure, victims typically experience a phase of decreased oxygen in the blood (hypoxemia). This phase is usually followed by re-oxygenation when the victim is removed from the toxic environment and oxygen administered. It also occurs when COHb is broken down and replaced with normal hemoglobin. The effects of CO-mediated hypoxemia are dependent upon any underlying disease that might be present (such as emphysema or heart disease).(7)

These periods of hypoxemia often result in the formation of dangerous chemicals called ˙free radicals,Ó which are highly reactive chemical compounds and cause cellular damage.(8,9) The increase in free-radical compounds results in oxidative stress, which damages body cells and is associated with the development of many diseases, including atherosclerosis, Parkinson's disease and Alzheimer's disease.(10) Thus, oxidative stress can cause injury to oxygen-sensitive tissues, such as the brain and the heart, beyond those caused by the initial hypoxemic insult.

CO poisoning can occur following acute and chronic exposures, which can result in long-term and often permanent problems. Although a well-fitted, self-contained breathing apparatus (SCBA) can protect the firefighter from environmental gases, the SCBA is often not worn through all phases of fire operations. It's not uncommon to see COHb levels up to 5% during the overhaul phase of operations when the SCBA is often removed.(11) Keep this in mind during rehab operations.

CO & the Heart

The heart is highly dependent on a constant supply of oxygen to function normally. Thus, the heart is highly susceptible to decreases in available oxygen. As discussed above, myocardial injury results from tissue hypoxia, as well as cellular damage due to the release of free radicals.

Victims of moderate to severe CO poisoning are at increased risk of developing cardiovascular complications.(12) In fact, in one study, CO from cigarette smoking caused ECG changes (ST segment depression) in people undergoing general anesthesia.(13) The cardiovascular complications of CO occur in all age groups, regardless of the patient's underlying health status.

In a 2005 study, researchers in Minneapolis studied 230 victims of CO poisoning and found that myocardial injury is common in moderate to severe CO poisoning.(14) In this study, two groups of patients were identified. The first group of patients was younger (average age 43 years) and had few cardiac risk factors. The second group was older (average age 64 years) and had more cardiac risk factors. In this study, the following factors were found as predictors of myocardial injury:

>Male gender;

>Hypertension; and

>Altered mental status (Glasgow Coma scale score of less than 14)

Interestingly, cigarette smoking lowered the relative risk of myocardial injury.(14)

Myocardial damage following CO poisoning has been seen in children.(15) In one study of pediatric CO poisoning, the risk of death decreased with hyperbaric oxygen therapy.(16)

Although most of those studies detailed above address immediate deaths from CO poisoning, other research is starting to demonstrate that long-term mortality may be related to both acute and chronic CO exposure.

In a Swedish study, researchers measured COHb levels in men who never smoked and correlated these with subsequent mortality. The COHb levels in the ˙never smokedÓ category ranged from 0.13%Ï5.47%. Those who never smoked and had COHb levels in the top quartile (25%) had a significantly higher incidence of cardiac events and deaths, compared with those in the lowest quartile. Researchers concluded the incidence of cardiovascular disease and death in non-smokers was related to COHb levels and suggested measurement of COHb levels should be a part of risk screening for cardiovascular disease.(17)

In a prospective study of 230 victims of moderate to severe CO poisoning, 85 patients (37%) had an associated myocardial injury.(18) These patients were followed for an average of 7.6 years after their initial poisoning. Interestingly, of the 85 who had myocardial injury, 32 (38%) eventually died. In contrast, only 22 (15%) of the 145 patients who didn't sustain myocardial injury eventually died. According to researchers, ˙While the precise mechanism for the increase in mortality is not clear, cardiovascular death was much more common (44% vs. 18%) among patients who initially sustained myocardial injury.Ó(18)

CO & the Brain

Like the heart, the brain is highly dependent upon a constant supply of oxygen. CO poisoning can interrupt oxygen delivery to the brain, causing brain hypoxia, which is later followed by oxidative stress. The detrimental effects of hypoxia and oxidative stress can be temporary or permanent.

Both acute and chronic neurological problems have been documented following CO poisoning, regardless of whether the CO exposure is acute or chronic. It's believed the mechanism of brain injuries is related to the production of free radicalsƒprimarily nitric oxide (NO). NO is normally found in the body and causes vasodilation, and can injure or kill cells through oxidative stress. NO levels are increased with CO exposure.(19)

The vast majority of NO is converted to a substance called methemoglobin (metHb). MetHb cannot carry oxygen. Increases in COHb from CO exposure and production of metHb from NO production secondary to CO exposure combine to significantly decrease the oxygen-carrying capacity of the blood, thus worsening hypoxemia following oxygen exposure.

Numerous neurological findings have been reported following CO exposure. These are primarily affective (mood) and cognitive (thought) in nature. In a study of 127 CO-poisoned patients, researchers found depression and anxiety were common; in fact, both were present in 45% of patients at six weeks and in 44% of patients at six months. Depression and anxiety were initially higher in patients whose CO exposure was due to a suicide attempt. However, at 12 months post-exposure, no difference in anxiety and depression levels was noted between those exposed to CO accidentally or as a suicide attempt.(20)

A phenomenon called ˙delayed neurologic syndromeÓ (DNS) has been identified as a complication of acute and chronic CO poisoning.(21) In DNS, recovery from the initial CO poisoning is seemingly apparent only to have the victim develop behavioral and neurological deterioration anywhere from two to 40 days later. The true prevalence of DNS is uncertain, with estimates ranging from 1Ï47% after CO poisoning. Patients who have more symptoms initially appear more apt to develop DNS. In addition, DNS is more common when there's a loss of consciousness in the acute poisoning.

The signs and symptoms of DNS are listed inFigure 2:Signs and Symptoms of Delayed Neurologic Syndrome. DNS has also been reported in children.(22) Scientific studies are mixed as to whether hyperbaric oxygen therapy prevents DNS.(23,24) Other neurologic complications, such as Parkinsonism (findings that mimic Parkinson's disease), have been reported with DNS.(25)

Taking Precautions

Most on-duty, fire-related deaths result from cardiovascular disease. Certainly, general cardiovascular risk factorsƒsuch as smoking, obesity, lack of exercise and dietary indiscretionƒcontribute to the disease. Thus far, studies of duty-related deaths haven't identified employment as a particular risk factor for the development of cardiovascular disease and ultimately death.(26) However, these studies haven't looked at the effects of CO poisoning (both acute and chronic) as a confounding variable in first responder duty-related deaths. Thus, because EMS personnel will soon be routinely responding to fire scenes to participate in rehab and medical operations, personnel must have an understanding of all possible effects of CO exposure.

In addition, chronic exposure to CO-induced free radicals may, in fact, be a major occupational risk factor for cardiovascular disease and early death. Exposure to cyanide and other toxic gases may compound the effects of CO. EMS personnel should minimize, as much as possible, their exposure to CO. In addition, more research is needed to determine whether there's a true link between occupational CO exposure and the development of cardiovascular and neurologic disorders among providers.


1. Fahy RF. ˙U.S. Firefighter fatalities due to sudden cardiac death, 1995Ï2004.Ó National Fire Protection Association. Quincy, Ma., June 2005.<A href=" OSCardiacDeath.pdf? PDF files assets http:>

2. ˙Firefighter Fatality Retrospective Study, April 2002.Ó Federal Emergency Management Agency, U.S. Fire Service, National Fire Data Center: TriData Corp. Arlington, Va. 2002.

3. Kales SN, Soteriades ES, ChristophiCA , et al. ˙Emergency duties and deaths from heart disease among firefighters in the United States.Ó . New England Journal of Medicine. 2007;356:1207Ï1215 .

4. Roberts MA, O'Dea J, Boyce A, et al. ˙Fitness levels of firefighter recruits before and after a supervised exercise training program.Ó . Journal of Strength and Conditioning Research. 2002;16:271Ï277 .

5. Clark S, Rene A, Theurer WM , et al. ˙Association of body mass index and health status in firefighters.Ó. Journal of Occupational Environmental Medicine. 2002;44:940Ï946 .

6. Bernard C. ˙Lecons sur les Effets des Substaces Toxiques et Medicamenteuses.Ó. J-B Bailliere et Fils. 1857;Paris .

7. Mannatoni PF , Masini VE . ˙Carbon monoxide: The bad and the good side of the coin, from neuronal death to anti-inflammatory activity.Ó . Inflammatory Research. 2006;55:262Ï273 .

8. Zang J, Piantadosi Ca. ˙Mitochondrial oxidative stress after carbon monoxide hypoxia in the rat brain.Ó. Journal of Clinical Investigations. 1992;90:1193Ï1199 .

9. Van der VaartH, Psotma DS, Timens W, etal. ˙Acute effects of cigarette smoke on inflammation and oxidative stress: A review.Ó. Thorax. 2004;59:713Ï721 .

10.Rice-Evans CA , Gopinathan V. ˙Oxygen toxicity, free radicals and antioxidants in human disease: Biochemical implications in atherosclerosis and the problems of premature neonates.Ó . Biochemical Essays. 1995;29:39Ï63 .

11. Dickinson, ET. Personal communication, May 7, 2007.

12.Williams J, Lewis RW, Kealey GP. ˙Carbon monoxide poisoning and myocardial ischemia in patients with burns.Ó Journal of Burn Care and Rehabilitation. 1992;12:210Ï213 .

13. Woehick HJ, Connolly LA, Cinquegrani MP , et al. ˙Acute smoking increases ST depression in humans during general anesthesia.Ó. Anesthesia Analog. 1999;89:856Ï860 .

14. Satran D, Henry CR, Adkinson C, et al. ˙Cardiovascular manifestations of moderate to severe carbon monoxide poisoning.Ó . Journal of the American College of Cardiology. 2005;45:1513Ï1516 .

15. Gandini C, Castoldi AF, Candura SM, et al. ˙Cardiac damage in pediatric carbon monoxide poisoning.Ó . Clinical Toxicology. 2001;39:45Ï51.

16. Chou KJ, Fisher JL, Silver EJ. ˙Characteristics and outcome of children with carbon monoxide poisoning with and without smoke exposure referred for hyperbaric oxygen therapy.Ó . Pediatric Emergency Care. 2000;16:151Ï155 .

17. Hedblad B, Engstr·m, Janzon E, et al. ˙COHb% as a marker for cardiovascular risk in never smokers: Results from a population-based cohort study.Ó . Scandinavian Journal of Public Health. 2006;34:609Ï615 .

18. Henry CR, SatranD, Lindgren B, et al. ˙Myocardial injury and long-term mortality following moderate to severe carbon monoxide poisoning.Ó . JAMA. 2006;295:398Ï402 .

19. Ischiropoulos H, Bears MF, Ohnishi ST, et al. ˙Nitric oxide production and perivascular tyrosine nitration in brain after carbon monoxide poisoning in the rat.Ó . ;Journal of Clinical Investigation. 1996;97:2260Ï2267 .

20. Jasper BW, Hopkins RO, Van Duker H, et al. ˙Affective outcome following carbon monoxide poisoning.Ó . Cognitive Behavioral Neurology. 2005;18:127Ï134 .

21. Raj RS, Abdurahiman P, Jose J. ˙Delayed neurologic syndrome in carbon monoxide poisoning.Ó. Journal of Association of Physicians in India. 2006;54:955Ï956 .

22. Kondo A, Saito Y, Seki A, et al. ˙Delayed neuropsychiatric syndrome in a child following carbon monoxide poisoning.Ó. Brain and Development. 2007;29:174Ï177 .

23. Gilmer B, Kilkenny J, Tomaszewski C, et al. ˙Hyperbaric oxygen does not prevent neurologic sequelae after carbon monoxide poisoning.Ó . Academic Emergency Medicine. 2002;9:1Ï8 .

24. Thom S, Taber RL, Mendiguren II, et al. ˙Delayed neuropsychiatric sequelae after carbon monoxide poisoning: Prevention by treatment with hyperbaric oxygen.Ó . Annals of Emergency Medicine. 1995;25:474Ï480 .

25. Lassinger BK, Kwak C, Walford RL, et al. ˙A typical Parkinsonism and motor neuron syndrome in a biosphere 2 participant: A possible complication of chronic hypoxia and carbon monoxide toxicity. Movement Disorders. 2004;19:465Ï469 .

26. Haas NS, Gochfeld M, Robson MG. ˙Latent health effects in firefighters.Ó . International Journal of Occupational and Environmental

27. Henry CR, Satran D, Lindgren B, et al. ˙Myocardial injury and long-term mortality following moderate to severe carbon monoxide poisoning.Ó. JAMA. 2006;295:398Ï402 .

Bryan Bledsoe, DO, FACEP, is a board-certified emergency physician and an author. A former EMT, paramedic and paramedic instructor, Bledsoe has written numerous EMS textbooks, including Brady's paramedic textbook series. He's a frequent contributor to JEMS and a regular speaker at EMS conferences worldwide.

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