A 65-year-old man is brought to the emergency department due to chest pain and shortness of breath for 1 hour. Prior to the onset of symptoms, he was preparing steak on an indoor charcoal grill. He has never had similar symptoms before. He takes metformin for his diabetes. Temperature is 37 C (98.6 F), blood pressure is 120/78 mm Hg, pulse is 114/min, and respirations are 24/min. Oxygen saturation is 96% on room air. On examination, the patient is drowsy and confused but acknowledges chest discomfort. Pupils are mid-sized and reactive to light. The chest has bilateral crackles. Cardiovascular examination reveals a normal S1 and S2 and no murmur or gallop. Neurologic examination shows no localizing weakness. ECG reveals sinus tachycardia with T-wave inversion in anterior leads. Cardiac troponin I level is elevated. Venous lactate is elevated. Chest x-ray reveals bilateral infiltrates. Emergency cardiac catheterization shows no acute coronary occlusion. Which of the following is the best next step in management?
Carbon monoxide poisoning | |
Epidemiology |
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Manifestations | Mild-moderate
Severe
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Diagnosis |
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Treatment |
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ABG = arterial blood gas. | |
This patient with chest pain, ECG changes, elevated troponin, and bilateral radiographic infiltrates has myocardial ischemia and pulmonary edema. Given his cardiac catheterization showing no acute coronary occlusion and symptom onset while grilling over charcoal, he likely has acute carbon monoxide (CO) poisoning induced–myocardial infarction (MI).
CO binds to hemoglobin with great affinity, displacing oxygen (O2) to create carboxyhemoglobin. This reduces O2-carrying capacity, decreases O2 unloading in tissues (hemoglobin dissociation curve left shift), and impairs O2 utilization (disrupted mitochondrial oxidative phosphorylation). Accordingly, while mild CO poisoning presents nonspecifically (eg, headache [most common], nausea, dizziness), severe CO poisoning can cause:
Cerebral hypoxia: Drowsiness, confusion, seizures, syncope, coma
Lactic acidosis: Elevated lactate (impaired oxygen utilization)
Myocardial injury: Ventricular arrhythmias, myocardial ischemia (ECG changes, hypertroponinemia even without obstructive coronary lesions), pulmonary edema (cardiac dysfunction or CO-induced alveolar damage).
Acute MI is reported in 1/3 of patients with CO poisoning and is associated with increased mortality.
Diagnosis of CO poisoning is best confirmed via co-oximetry of arterial blood gas showing elevated carboxyhemoglobin levels (>3% for nonsmokers, >10% for smokers) in a symptomatic patient. Treatment with 100% O2 by nonrebreather facemask increases blood O2 level and enhances CO removal via the lungs.
(Choice A) Benzodiazepines are sometimes used in managing cocaine toxicity, which can cause MI. However, dilated pupils and hyperstimulation (not drowsiness) would be expected.
(Choices C and F) CT scan of the chest and transesophageal echocardiogram (TEE) are indicated if pulmonary (eg, interstitial lung disease) or cardiac (eg, valve abnormalities) processes are suspected. TEE is also used in patients with hemodynamic instability and concern for aortic dissection, which can cause chest pain and ECG changes but usually causes mediastinal widening on x-ray. This patient's presentation can be explained by CO poisoning; these studies risk further delaying management of CO poisoning without providing useful information.
(Choice D) Pulmonary embolism can cause chest pain, dyspnea, ECG changes, hypertroponinemia, and rarely bilateral infiltrates. However, lactate elevation would be uncommon in the absence of a massive embolism causing obstructive shock and hypoperfusion. His oxygen saturation level (>90%) should not make him drowsy either. An ABG to check for carboxyhemoglobin level is much easier (and less contrast exposure) to obtain than CT angiogram.
(Choice E) Metformin-induced lactic acidosis is unlikely to occur acutely and is not classically associated with MI. Although stopping metformin is necessary in this hospitalized patient with lactic acidosis, evaluation for CO poisoning is indicated.
Educational objective:
Carbon monoxide poisoning disrupts oxygen delivery and usage, which can cause clinical manifestations of myocardial ischemia. Elevated carboxyhemoglobin levels confirm the diagnosis. Severe cases require hyperbaric oxygen therapy.