A group of employees present from the billing office complaining of headache and dizziness. Because it’s been so cold recently, one of them brought in a space heater to keep under her desk.

What are you concerned about? How would you go about working this up? What would the treatment be?

Carbon monoxide poisoning can manifest with a variety of non-specific signs and symptoms, depending on the length of exposure, proximity of exposure, patient age and pre-exisiting medical conditions. Headache is by far the most common symptom, others can include nausea, vomiting, angina, depressed level of conciousness, hypotension, convulsions, coma, dysrhythmias, and death. Cherry red skin, owing to the color of carboxyhemoglobin, is an autopsy finding, almost never clinically present. In developed nations, CO remains the most common cause of acute poison-related deaths. Its danger is related to the fact that it is invisible, odorless, and non-irritating.

CO adverse effects are due to its binding to iron found in hemoglobin, myoglobin, and intracellular cytochrome. It binds to hemoglobin with a much higher affinity (250 times) than does oxygen, and shifts the oxygen dissociation curve so that the bound oxygen is held tighter.  It disrupts the normal function of myoglobin to store and transfer oxygen in muscle (such as the heart), and binds to intracellular cytochromes leading to inhibition of oxidative phosphorylation (similar to cyanide), thereby preventing both cellular oxygen delivery and intracellular oxygen utilization. The most adversely affect organs are those with high oxygen utilization, such as the brain and the heart.

Treatment involves removing the patient from continued exposure and instituting oxygen therapy with a NRB mask. Intubate patients as needed for depressed conciousness and treat with 100% oxygen. Place the patient on a cardiac monitor to monitor for dysrhythmias. As HbCO absorbs light almost identically to oxyhemoglobin, pulse oximetry will not reflect a drop as HbCO level rises.  Use a pulse CO-oximetry unit to screen for CO toxicity at the bedside (located in the Cardiac Room at Elmhurst). Continue 100% O2 therapy until the patient is asymptomatic and HbCO levels are below 10%. In patients with cardiovascular or pulmonary compromise, lower thresholds of 2% have been suggested.

Consider immediate transfer of patients with levels above 40% or with CV or neurologic impairment to a hyperbaric facility. Persistent impairment after 4 hours of normobaric O2 therapy necessitates transfer to a hyperbaric center. Pregnant patients with lower HbCO levels (above 15%) should also be considered for hyperbaric treatment.