Chest pain is a common symptom in acute myocardial infarction and a common cause of admission to medical departments. Approximately 10,000 people have an acute myocardial infarction in Norway each year, and patients with an established history of coronary artery disease are at increased risk of suffering a further myocardial infarction (1, 2).
The diagnosis of acute myocardial infarction is based on a rise and/or fall in the cardiac marker troponin as well as at least one of the following additional criteria a) ischaemic symptoms, b) ECG changes, c) imaging evidence of loss of viable myocardium or new regional wall motion abnormality, or d) identification of intracoronary thrombus by angiography or autopsy (3). Our patient fulfilled the diagnostic criteria for acute myocardial infarction if his chest pain was interpreted as ischaemic symptoms or the queried hypokinesia on echocardiography was considered conclusive.
However, in this case, the cause was not coronary atherothrombosis. In this situation of carbon monoxide poisoning, there was an imbalance between oxygen demand and supply in the myocardium since oxygen was displaced from haemoglobin in the blood. The myocardial infarction can be defined as a type 2 infarction.
In a busy emergency department, it is easy to follow the first diagnostic assumption, which is often 'inherited' from the referring doctor or ambulance service. Our patient was admitted with typical clinical findings of acute coronary syndrome, with relief provided by glyceryl trinitrate in the ambulance. Although the patient himself suspected carbon monoxide poisoning and communicated this, the findings and test results were interpreted as confirmation of coronary syndrome. This type of confirmation bias is probably recognisable to everyone working in emergency medicine, but is something we should always be alert to. A thorough case history with probing questioning about relevant information is essential for correct diagnosis and treatment, but can unfortunately be easily missed on a busy shift. Our case report illustrates the importance of being attentive to the patient's own assumption about the diagnosis.
Carbon monoxide (CO) is an odourless, colourless and non-irritant gas produced by the incomplete combustion of organic material due to insufficient oxygen supply. Carbon monoxide poisoning is likely to be responsible for over half of all fatal cases of poisoning worldwide (4). Carbon monoxide that is not accompanied by smoke can only be detected using a CO detector, but should be suspected in all fires and when combustion devices are used in confined spaces.
Symptoms of carbon monoxide poisoning can develop gradually over minutes to hours. Signs and symptoms of hypoxia are most prominent in the acute phase. The heart and brain have a high oxygen consumption and are thus most sensitive to oxygen deficit with the earliest impact on organ function. Central nervous system symptoms, such as headache and dizziness, occur frequently. Other common symptoms of hypoxaemia are tachypnoea and dyspnoea. Non-ST-elevation myocardial infarction (NSTEMI) on ECG or type 2 infarction are rarer, but not uncommon (5).
Patients with acute carbon monoxide poisoning usually have HbCO levels above 10 % (6), but severity correlates poorly with the levels measured because these decrease over time, particularly with oxygen treatment. HbCO levels above 40 % are reported to be fatal (7, 8), although many people have survived with higher levels. Carbon monoxide binds to the oxygen binding site on the haemoglobin molecule with much higher affinity than oxygen and thus blocks normal oxygen transport in the blood.
Oxygen is vital for the maintenance of aerobic metabolism, enabling energy-carrying adenosine triphosphate (ATP) molecules to be created. This ATP production takes place mainly in the mitochondria. Carbon monoxide also binds to cytochromes, myoglobin and guanylyl cyclase (9). Binding to cytochrome 3A and cytochrome C-oxidase in the mitochondria blocks oxidative metabolism. This results in the production of reactive oxygen compounds, leading to oxidative stress. Carbon monoxide competes with nitric oxide (NO) for binding to proteins, which in turn results in increased NO levels. Reactive oxygen compounds and nitric oxide appear to play an important role in the development of oxidative brain injury with peroxidation and demyelination, and may explain the delayed neurological sequelae experienced by some patients following severe poisoning.
Most pulse oximeters do not differentiate between oxyhaemoglobin (HbO2) and carboxyhaemoglobin (HbCO) and therefore cannot be used for diagnosis. In this particular case, the pulse oximeter showed oxygen saturation (SpO2) of 100 %, even though 27.4 % of haemoglobin was occupied by carbon monoxide.
The treatment of carbon monoxide poisoning is primarily with normobaric oxygen. Carbon monoxide is excreted via the lungs once exposure stops, and elimination follows the concentration gradient. In addition, oxygen will compete for the binding sites and facilitate elimination. The higher the oxygen concentration, the faster excretion will take place. The half-life of HbCO in the blood of patients on room air (21 % oxygen) is 4–6 hours, but this decreases to approx. 1.5 hours with the administration of 100 % oxygen (10).
If the amount of oxygen is increased with the use of a pressure chamber, which is referred to as hyperbaric oxygenation, the half-life will decrease further to approx. 20 minutes with 100 % oxygen at 3 atmospheres of pressure, equivalent to a depth of 20 metres underwater. A pressure tank or hyperbaric oxygen therapy has not been shown to reduce mortality in the acute phase because normobaric oxygen therapy is enough to counter the hypoxia, but the method has been used to limit the delayed neurological sequelae (9). This is controversial though, and the results of clinical trials have not been conclusive (11). The treatment rapidly reduces the concentration of HbCO, but does not assist in reducing the concentration of oxygen radicals.
Although treatment in modern pressure chambers is safe on the whole, any hyperbaric therapy is associated with some risk of barotrauma (ear and sinus injuries, pneumothorax) and oxygen toxicity (12, 13). Hyperbaric oxygen therapy is still used in Norway, but the trend is to restrict who is offered this treatment. According to the guidelines of the Norwegian Poisons Information Centre and Oslo University Hospital, hyperbaric oxygen therapy is recommended if HbCO > 25–30 % (for pregnant women HbCO > 15 %), in patients with loss of consciousness, severe metabolic acidosis (pH <7.25) or evidence of end‐organ damage (e.g. ECG changes, elevated cardiac markers, respiratory failure, neurological deficit or altered mental status).
Our patient was not assessed for hyperbaric oxygen therapy. Even though his HbCO levels were high enough, he did not have metabolic acidosis or loss of consciousness while admitted, and it was a long way to travel to a chamber. New treatment principles that have not yet been fully clarified include normocapnic hyperventilation, in which carbon dioxide is added to inspired air to increase respiratory minute volume. This lowers the half-life of carbon monoxide by an equivalent amount to a pressure tank, but without causing such a high oxygen load. Medicinal treatment of the inflammatory processes with steroids has also been proposed (14), but this has also not yet been studied in enough depth for it to be recommended as routine practice.