Toxicology Case Files from the Utah Poison Control Center
Take Home Points
- Carbon monoxide (CO) exposures increase in winter months and are characterized by headache, dizziness, and nausea in mild cases.
- Consider CO poisoning when other “flu-like” symptoms such as fever, cough, and sore throat are absent.
- Carbon monoxide poisoned patients should be evaluated with an EKG, BNP, and troponin as myocardial injury may occur without typical symptoms of myocardial ischemia.
- Significant myocardial injury may occur in healthy patients without coronary artery disease.
- Carbon monoxide levels are not predictive of myocardial injury.
- Call the poison center for assistance with any CO exposure at 1-800-222-1222.
Carbon Monoxide Poisoning
Carbon monoxide is an odorless, colorless gas produced from the combustion of any carbon-based fuel (e.g. gasoline, propane, wood). It avidly binds to hemoglobin and other intracellular enzymes such as cytochrome oxidase leading to decreased oxygen delivery and mitochondrial damage.
Symptoms are those expected of hypoxia (headache, confusion, dizziness, nausea) but may be more serious (syncope, seizures, coma) or involve direct tissue toxicity (rhabdomyolysis, myocardial toxicity, dysrhythmias).
Standard pulse oximetry will be falsely normal. Specialized pulse co-oximeters are available but are not commonly used in hospitals but are often used by EMS. Blood gas analysis with co-oximetry and direct measurement of carboxyhemoglobin is required for definitive diagnosis. However, it is important to recognize that carbon monoxide levels do not correlate well with toxicity.
At a minimum, all patients should receive 100% oxygen until symptoms improve and carbon monoxide is expected to be eliminated. In general, the half-life of carbon monoxide is about 4.5 hours on room air, 90 minutes on 100% oxygen, and 20-30 minutes with hyperbaric oxygen.
Indications for hyperbaric oxygen therapy are not well established but may be considered in any patient with significant symptoms or more specifically with a CO > 25% (15% in pregnancy), syncope, any altered mental status, evidence of cardiac toxicity, or acidosis.
A 60 year-old male was brought to the ED after being found unresponsive in his car. He had been burning coals for heat and had an area of partial thickness burn to his head.
Carboxyhemoglobin was 25% by pre-hospital pulse co-oximetry and 22% by blood co-oximetry in the emergency department. The patient was drowsy and he required stimulation to wake up but could answer questions appropriately.
He was transferred to a facility capable of providing hyperbaric oxygen therapy. He had an episode of non-sustained ventricular tachycardia during hyperbaric treatment. His EKG reportedly otherwise did not show ischemic changes. Serial troponin measurements increased from 0.24 > 7.53 > 12.5 ng/ml. An echocardiogram demonstrated segmental wall motion abnormalities. He underwent cardiac catheterization with successful stenting of a 95% occluded left anterior descending artery lesion.
Carbon Monoxide Cardiotoxicity?
Carbon monoxide may cause cardiotoxicity in children, healthy adults, and those with underlying cardiac disease.
There are a variety of purported mechanisms including CO binding to cardiac myoglobin, inhibition of mitochondrial cytochromes, systemic vasodilation leading to hypotension and hypoperfusion, and oxidative stress during reperfusion.
Potential clinical effects include ischemic EKG changes, arrhythmias, chest pain, and dyspnea. Interestingly, significant myocardial damage can occur without typical anginal symptoms.
Initial diagnostic evaluation of CO cardiotoxicity should include an EKG and troponin. BNP may also be useful as it correlates with poor neurologic outcome better than troponin (Moon 2017). If these tests are abnormal, further investigation may be made via echocardiogram, myocardial perfusion imaging, or cardiac catheterization as indicated. As with other findings in CO poisoning, CO levels do not correlate well with markers of cardiac injury such as troponin.
A variety of echocardiogram findings may be present in patients with elevated troponin due to CO (Yong 2017). In this series echo findings were variable: normal (59.4%), global dysfunction (25%), Takotsubo cardiomyopathy (6.3%), and wall motion abnormalities in the LAD territory (9.4%).
Treatment of CO cardiotoxicity is supportive and as in all CO cases should be treated with 100% oxygen at a minimum. Whether cardiotoxicity is improved by hyperbaric oxygen treatment is not clear. Nor is it clear if cardiotoxicity should be a separate indication for hyperbaric oxygen. On the other hand, those with cardiotoxicity may be at risk for complications while in the hyperbaric chamber as in this patient’s case.
Standard treatments for acute coronary syndrome, heart failure, and cardiogenic shock should be given for their usual indications.
Yong Sung Cha, Hyun Kim, Yoonsuk Lee, Woocheol Kwon, Jung-Woo Son, Hyun Youk, Hyung Il Kim, Oh Hyun Kim, Kyung Hye Park, Kyoung-Chul Cha, Kang Hyun Lee & Sung Oh Hwang (2018) Evaluation of relationship between coronary artery status evaluated by coronary computed tomography angiography and development of cardiomyopathy in carbon monoxide poisoned patients with myocardial injury: a prospective observational study, Clinical Toxicology, 56:1, 30-36, DOI: 10.1080/15563650.2017.1337910
Cristiano Gandini, Anna F. Castoldi, Stefano M. Candura, Carlo Locatelli, Raffaella Butera, Silvia Priori & Luigi Manzo (2001) Carbon Monoxide Cardiotoxicity, Journal of Toxicology: Clinical Toxicology, 39:1, 35-44, DOI: 1081/CLT-100102878
Jeong Mi Moon, Byeong Jo Chun, Min Ho Shin & Seung Do Lee (2018) Serum N-terminal proBNP, not troponin I, at presentation predicts long-term neurologic outcome in acute charcoal-burning carbon monoxide intoxication, Clinical Toxicology, 56:6, 412-420, DOI: 10.1080/15563650.2017.1394464
Call Utah Poison Control Center (1-800-222-1222)
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The UPCC is a 24-hour resource for poison information, clinical toxicology consultation, and poison prevention education. The UPCC is a program of the State of Utah and is administratively housed in the University of Utah, College of Pharmacy. The UPCC is nationally certified as a regional poison control center.