Research Applied to Clinical Practice
we head into Fall, many people will be getting their wood stoves, fireplaces and other
heating systems ready for the cold Minnesota winter. People are also planning to grill in
their garages, going ice fishing in the "ice houses", and using any other way to
produce warmth. With the use of heating devices, which produce heat via combustion, comes
the risk of Carbon Monoxide (CO) Poisoning.
CO has been called the silent killer and has been the cause of approximately 5,000 deaths annually, with 2 to 5 times that requiring treatment (Krenzelok, Roth, & Full, 1996). Even with treatment the devastating sequalle that can accompany CO poisoning can be life changing. These include chorea, rigidity, dementia, myoclonus, impaired sensory function, seizures, and gait dysfunction. There can also be permanent cardiac damage due to the hypoxia involved in the poisoning process (Huston, 1996).
CO is an odorless, colorless and tasteless gas that results from incomplete combustion of fuels (i.e., coal, wood, gasoline). Once inhaled it binds quickly and tightly to the hemoglobin (Hgb), crowds out the oxygen and studies have shown CO can bind 200 times stronger than oxygen (Huston, 1996). Since the Hgb can no longer carry the oxygen the patient becomes hypoxemic and anoxic. Also the CO binds with myoglobin in the muscles and interferes with cellular metabolism causing metabolic acidosis (Huston, 1996).
Normal carboxyhemoglobin (HbCO) levels are 0% to 3% for non-smokers and 3% to 8% for smokers. Levels of 10% to 20% causes headaches, nausea, vomiting and dyspnea. 30% to 40% causes severe headaches, syncope, tachy-arrhythmias. Greater than 40% causes Cheyne-Stokes respiration or respiratory failure, seizures, unconsciousness, permanent brain damage, cardiac arrest and even death (DiDonna, 1997). Studies have shown that a CO concentration of even 0.05% can be fatal in less than 30 minutes (Huston, 1996).
Because of the vagueness of the symptoms and their similarity to flu-like symptoms (N-V, dizziness, headache, etc.) CO poisoning is often misdiagnosed (Roy, & Crawford, 1996). Also, even if HbCO is present it can not be diagnosed with a simple pulse oximetry device because the displayed saturation levels equals the sum of the oxyhemoglobin and carboxyhemoglobin (Vegfors & Hennmarket, 1991).
So if a patient comes to the EC or UC and you suspect CO poisoning what should you do? First and foremost, the patient needs high flow, high concentration O2, preferably a non-rebreather mask at 15 liters per minute, also a large bore IV. Prepare for blood draws (ABG, CBC, Lytes, CPK, Lactate, & Carboxyhemoglobin), a urine sample is also useful to rule out rhabdomyolysis (cardiac muscle breakdown secondary to the myoglobin damage from CO). Other treatment modalities may include a CXR, cardiac monitoring and possibly Mannitol (1-2G/kg) to help decrease the cerebral edema accompanying the CO poisoning. Lastly, but probably the most effective treatment is transfer of the patient to a hyperbaric oxygen unit (HBO), this is clearly indicated when the patient is very symptomatic and or the HbCO is 25% or greater.
HBOs help speed up the CO washout by providing high O2 concentrations at increased atmospheric pressures. The half life of CO is 240 minutes at room air, but with 100% O2 it is 60 minutes. Other patients who should be considered for HBO therapy is pregnant patients and those with cardiac history or any loss of consciousness.
Currently in the community most fire departments and utility companies have and are trained in use of CO measuring devices. Also home monitoring/alarm systems are readily available (usually less than $75) at most hardware and retail stores. But, we also need to be educating the public to have their heating systems checked yearly by trained personnel before use, and to provide proper ventilation when using other forms of heat producing combustion devices.
DiDonna, T.A. (January, 1997). Actionstat: Carbon monoxide
poisoning. Nursing 97. p 33.
"Research Applied to Clinical Practice: Carbon
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