Carbon monoxide (CO) is a colourless, odourless gas produced as a by-product of combustion. Poisoning occurs by inhalation, either accidentally or intentionally (suicide attempt). CO poisoning is responsible for an estimated 40,000 emergency department visits and 1,000 accidental deaths annually in the United States alone.
CO binds to haemoglobin in red blood cells at the sites usually used to carry oxygen to tissues. Oxygen, and especially hyperbaric oxygen, accelerates the clearance of CO from the body, thereby restoring oxygen delivery to sensitive tissues such as brain and heart. This has traditionally been considered the mechanism of benefit of HBO2. However, research published in the past few years has demonstrated a number of other mechanisms of toxicity from CO. Blood vessel (vascular) injury from CO has been demonstrated to result from CO-induced production of nitric oxide-derived oxidants and cellular injury from activated white blood cells (neutrophils). CO also causes direct central nervous system cellular injury through mechanisms that include disturbance of energy metabolism and intracellular production of oxygen free radicals. In animal experiments, hyperbaric oxygen, but not normobaric oxygen (NBO2), has been demonstrated to block each of these mechanisms of toxicity.
The pathophysiology of Carbon Monoxide (CO) poisoning includes:
- Binding of CO to the haemoglobin molecule to form carboxyhaemoglobin
- Reduced oxygen delivery to the tissues
- Undefined cellular effects, as well as lipid peroxidation and cytochrome binding.
Hyperbaric Oxygen Therapy:
- Produces a rapid dissociation of CO from haemoglobin (the half-time for elimination of CO is reduced from over 5 hours with air to 23 minutes when the patient is given hyperbaric oxygen).
- Oxygen breathing at 3 atmospheres absolute (ATA) provides immediate delivery of dissolved oxygen in plasma in an adequate amount to support basic tissue metabolism, even when the amount of CO bound to haemoglobin is high