carbon monoxide poisoning

Cause

CO is a tasteless, odorless, and colorless gas that may cause a headache, weakness, dizziness, and nausea, along with tachycardia and tachypnea. Toxicity occurs owing to its effect on oxygen binding to the hemoglobin molecule; the gas binds to hemoglobin, forming COHb, with a much greater affinity to hemoglobin than oxygen. This reduces the oxygen-carrying capacity of hemoglobin and leads to cellular hypoxia. COHb increases the affinity of unbound hemoglobin for oxygen, thus causing a leftward shift in the oxyhemoglobin dissociation curve. Additionally, CO binds to the heme moiety of the cytochrome C oxidase in the electron transport chain and inhibits mitochondrial respiration. These effects cause a lower tissue and intracellular PO2 than would otherwise be expected for a given blood oxygen concentration. The hemoglobin concentration and the PO2 of blood may be normal, but the oxygen content of the blood is reduced significantly.

Carbon monoxide, a colorless and odorless gas, can be potentially fatal after exposure if not properly diagnosed and treated. Carbon monoxide poisoning is associated with:

  • Automobile exhaust
  • Inadequately ventilated heaters (hence most commonly occurring in the winter)
  • Methylene chloride ingestion (converts to CO hepatically)

Although it has no detectable odor, CO used in industrial processes is often mixed with other gases, such as ethyl mercaptan, that do have an odor for safety purposes. CO is a common industrial hazard resulting from the incomplete combustion of natural gas or any other carbonaceous material such as gasoline, kerosene, oil, propane, coal, or wood.

Pathophysiology

Carbon monoxide has several pathophysiological consequences on oxygen transport and utilization:

  • Carbon monoxide binds to heme with 240x the affinity of oxygen forming carboxyhemoglobinemia
  • Allosteric changes of the heme moiety prevent oxygen unloading peripherally
  • CO binds to various proteins affecting oxidative phosphorylation

Symptoms

In addition to a history consistent with CO exposure, patients with mild CO poisoning present with:

  • Headache (most common symptom)
  • Viral-like symptoms (e.g. dizziness, nausea, vomiting, malaise)
  • Altered mental status

Patients severely exposed to carbon monoxide typically present with:

  • Neuropsych symptoms: seizures, delirium
  • Cardiology symptoms: myocardial ischemia, arrhythmias
  • **Mortality **

Physical exam signs of carbon monoxide toxicity may include:

  • Tachycardia
  • Pallor or Cherry-red skin
  • Memory disturbance
  • Neuropsychiatric: emotional lability, impaired judgment
  • Pulmonary edema

Diagnosis

The diagnosis of carbon monoxide poisoning is dependent upon:

  • History
  • Physical exam
  • Arterial blood gases demonstrating elevated carboxyhemoglobin levels

Following the diagnosis of carbon monoxide poisoning, an electrocardiogram is recommended to detect for ischemia as myocardial infarction is a common complication.

Carboxyhemoglobin shifts the oxygen dissociation curve to the left, impairing the ability of heme to unload oxygen at the tissue level. This results in tissue hypoxia. The kidney responds to tissue hypoxia by producing more erythropoietin (EPO). EPO stimulates the bone marrow to differentiate more red blood cells. Chronic CO toxicity is a cause of secondary polycythemia.

Chronic tobacco smokers may have up to 15% carboxyhemoglobin at baseline.

Carbon monoxide saturation levels above 40% is considered to be severe exposure, whereas levels above 55% can potentially be fatal.

Management

The management of carbon monoxide poisoning includes:

  • Removal from the carbon monoxide source
  • 100% high-flow oxygen or a hyperbaric oxygen chamber (decreases the half life of CO)
  • Intubate if necessary