Carbon Monoxide Poisoning

Carbon Monoxide Poisoning – Intentional carbon monoxide poisonings used to be a common case for paramedics. Fortunately, since the early 1990s changes in motor vehicle efficiency made it more difficult for people to use this as a means of suicide. However, this does not preclude people from trying, or from people using older vehicles to poison themselves with carbon monoxide.

In most cases a diagnosis of carbon monoxide poisoning clear to the paramedic upon arrival at a scene due to the contraption set up in a vehicle with the exhaust fumes filling the car (that remains running). However, in some cases, the diagnosis of carbon monoxide poisoning is much less clear. For example, where a person has been working in close proximity to heavy machinery in a closed space, or where an internal exhaust pipe has been damaged causing carbon monoxide to leak into a vehicle. In these cases, the diagnosis of carbon monoxide poisoning is much less clear. ‘

Carbon monoxide in itself is a clolourless, odorless gas (although the exhaust/combustion residue will normally be identified).

Carbon Monoxide Signs and Symptoms

Signs of poisoning include: cherry red skin and mucous membranes as a result of bright red COHb (Thorn, Adams, Isselbacher and Petersdorf 1977, p. 693); confusion, dizziness, headache, visual disturbances, nausea, vomiting, early onset of fatigue with little physical exhaustion, coma, hyper-reflexia, convulsions, and arrhythmias. Acute exposure: depends on level of COHb. Generally no symptoms are experienced when COHb levels < 10% while levels > 60% associated with coma and cardiorespiratory arrest (Sanders 2001, p.610). Late symptoms include neuropsychiatric complications, which may develop weeks after exposure. These include memory loss, impaired intellect, and signs of cerebellar and mid-brain damage.

Oxygen SPO2 may falsely read as high as 99-100% because it is measuring the CO molecules combined with the Haem molecules and not Oxygen combined with the Haem molecules.

Carbon monoxide inhalation causes many noticeable physiological changes in a patient although it does not physically harm lung tissue, it causes a reversible displacement of oxygen on the haemoglobin molecule, forming carboxyhemoglobin (COHb). As a result, there are low circulating volumes of oxygen despite normal partial pressures and in addition it requires tissues to become very hypoxic before oxygen is released from haemoglobin to oxygenate cells.

Carbon monoxide poisoning causes anaemic hypoxia, which is where the blood oxygen partial pressure is normal, but there is a lack of normal haemoglobin (Hb) or altered haemoglobin used for oxygen carriage. In CO poisoning, CO molecules occupy the oxygen sites on the Hb, therefore making it difficult for oxygen to take its place on the Hb molecule. There are four oxygen carrying ‘carriages’ on one Hb molecule and all four of these can become occupied by O2, CO or CO2. CO has an affinity for Hb 200-250 times that of oxygen, this means that even low concentrations of inspired CO can result in tissue hypoxia, inadequate cellular oxygenation, inadequate cellular and organ function and eventually death

According to the Hong Kong College of Anaesthesiologists the ‘elimination ½ life of CO reduces from 250 minutes when breathing air to 59 mins breathing 100% O2 and 22 min when breathing 100% O2 at 2.2 atmospheres’ (Hong Kong College of Anaesthesiologists 2004).

Carbon Monoxide Treatment

Remove the patient away from the site of CO exposure as soon as safely possible. As with all burn injuries, the safety of the paramedics (and other rescuers) must be the first consideration in managing the victims of gaseous injury. Administration of 100% O2 is very important as this increases the partial pressure of inspired O2, which increases the chance of O2 binding to the Hb molecules and removing the CO.

The greater the amount of O2 in inspired air, the greater the partial pressure of oxygen (PaO2) in the alveoli and the higher the PaO2 in alveoli the greater the promotion of diffusion across the alveolus into the capillaries.The route of 100% O2 administration depends on the patient’s level of respiration. At a minimum, a patient suspected of suffering a CO inhalation poisoning should be on a non-rebreathing O2 mask at 14l/min and if respirations are inadequate the patient should be assisted as much as required with intermittent positive pressure ventilation (IPPV) via a resuscitation bag (Sanders 2002, pp 612).

If unconscious or unable to maintain his/her own airway, patient should be intubated and ventilated manually.  In severe poisoning assume cerebral oedema and treat accordingly. Although the use of hyperbaric oxygen is still debatable, the Hong Kong College of Anaesthesiologists believe that two categories of patients should be treated with hyperbaric oxygen. The ‘conscious patient with COHb level > 20% and a depressed level of consciousness who is able to maintain their own airway’ and ‘after the recovery of a patient’s consciousness after an initial COHb level of > 40%’ (Hong Kong College of Anaesthesiologists 2004).