Carbon monoxide poisoning is the second-leading cause of poisoning death after drugs. Carbon monoxide is a covert killer and it causes between 200 and 1000 deaths per year in the US. Here is what you should know to avoid poisoning from this colorless, tasteless, odorless, non-irritating gas.
A neighbor calls you on the phone and asks for help. Her husband’s having a seizure. Upon your arrival you detect an un-usual odor, like that around the air-port. In answer to your inquiry the patient’s wife states that it’s just the kerosene heater in the basement, to keep the pipes from freezing, and what business is it of yours anyhow?
The lady’s response seems a bit strange to you. You also notice the children are pale. Through further questioning you find the whole family hasn’t felt good since the weather became extremely cold, the day before. Your patient has no prior history of seizure activity and has always been in good health. never complaining
The mechanic from the shop next door comes over to your house and asks for
something for his “flu.” He is com-plaining of nausea and a headache. He mentions he’s been busy all day tun-ing cars in preparation for the winter. He states he’ll close early today and go on home. Between the flu and the noise inside the closed up garage, he really feels “worn out:’
Kerosene heaters and vehicle exhaust — what do these have in common? They produce CARBON MONOXIDE.
Carbon monoxide – The a covert killer
Carbon monoxide (CO) is a clear, odorless, toxic gas having a specific gravity of .97 (the specific gravity of air is 1.00). Carbon monoxide is formed by the incomplete combustion of organic (carbon containing) materials. This can be coal, kerosene, gasoline, wood or plastic to only name a few. As a matter of fact, carbon monoxide is itself flammable.
Given the right conditions, oxygen and intense heat, carbon monoxide will oxidize very rapidly to form carbon dioxide. This is the mechanism the fire service has come to call “back draft.” A poorly ventilated fire inside a closed structure rapidly consumes the available oxygen.
What remains are intense heat, and flammable products of combustion (carbon monoxide included). When a door or window is quickly opened the oxygen rich air rushes in and a back draft explosion results, pound for pound of fuel, a free burning fire, well supplied with oxygen produces considerably less carbon monoxide than its less dramatic, smoldering counterpart.
Suggested reading: The Anatomy Of Burn Injuries And Their Medical Treatment
A less obvious source of CO poisoning is the “safe” kerosene heaters used in so many homes these days. It must be emphasized, they are indeed safe —if the manufacturer’s instructions are followed. If the heater is to be used in a closed environment, the instructions state that the windows be left cracked to facilitate improved ventilation.
While the efficiency of these heaters is very high when they are adjusted properly, they still produce some carbon monoxide. The rapidity with which exposure produces symptoms and the relatively mild distress associated with those symptoms, coupled with ease of production (for example, an automobile engine) make carbon monoxide an unfortunately attractive choice of so many people for a suicide attempt.
Old automobile’s exhaust is approximately 1 to 7 percent carbon monoxide. In fact, this is such an effective means of self-destruction that over 50 percent the suicides yearly are committed by this means. Charcoal grills and hibachis used in unventilated areas have accounted for in excess of 40 documented deaths in recent years.
Physiological Effects
To understand the physiological effects of carbon monoxide poisoning, we will review what occurs during normal respiration. Oxygen rich air enters the lungs during inspiration. Here the oxygen migrates through the walls of the alveoli and combines chemically with hemoglobin in the blood to form oxyhemoglobin.
The blood then travels through the pulmonary vein to the heart which pumps it through the body’s arterial system, until it arrives adjacent to a cell deficient in oxygen. Here the oxygen-hemoglobin bond is broken and the oxy-gen migrates through the cell wall. Simultaneously, carbon dioxide, produced by cell metabolism, passes through the cell wall and combines chemically with the hemoglobin to form hemoglobin carbamate which then travels the circulatory system until it eventually returns to the lungs.
Upon reaching the alveoli, the car-bon dioxide-hemoglobin bond is broken, allowing the carbon dioxide to pass into the lungs and be expelled during exhalation. The process is then repeated.
This obviously is a fairly simple chemical process. Problems arise, how-ever, when a gas, for which hemoglobin has a higher affinity than oxygen, enters the lungs. Carbon monoxide is just such a gas. In fact, according to the NFPA (National Fire Protection Association)Fire Protection Handbook, carbon monoxide combines 210 times more readily with hemoglobin than does oxygen. In this case the resultant compound, carboxyhemoglobin, is carried throughout the body. Upon arrival at an oxygen deficient cell, no exchange of gasses occurs.
Therefore the cell retains the carbon dioxide, becomes anoxic, and dies. The mechanism of injury of car-bon monoxide poisoning is therefore hypoxia (oxygen deficiency) leading to asphyxiation.
Signs, Symptoms of Carbon Monoxide Poisoning
Based on tests by the EPA, an atmosphere of 50 parts per million CO will produce a carboxyhemoglobin level of 6.5 percent after three hours of exertion (such as at-tempting to escape from a burning building), In a structure fire, the car-bon monoxide level reaches 10,000 ppm within 14 minutes. One minute of exposure at this level is fatal.
Based on information obtained from a number of studies, the following signs and symptoms will be apparent in a patient suffering from carbon monoxide poisoning.
Carbon monoxide poisoning symptoms:
- At 10 to 20 percent carboxyhemoglobinemia (presence in blood of carboxyhemoglobin), cerebral hypoxia (inadequate oxygen to the brain) will cause the patient to become irritable. In an attempt to adequately profuse the brain, vasodilation will occur, leading to complaints of headache.
- At 20 to 30 percent, the patient will complain of a throbbing headache. Dyspnea (shortness of breath) upon moderate exertion will be apparent. The patient may appear to be pale.
- At 30 to 40 percent, the preceding signs and symptoms become more severe. Nausea with emesis (vomiting) will probably be noted; also complaints of malaise (“just feel bad”) and visual disturbances. Impaired thought processes may be noted in the form of loss of coordination and confusion.
- At 40 to 50 percent, the prior symptoms will intensify. Sinus tachycardia (rapid heartbeat) with increased myocardial (heart tissue) irritability evidenced by the presence of ectopic (abnormal) beats (both atrial and ventricular) will be noted on a heart monitor. Tachypnea (rapid breathing) will be noted. Syncope (fainting) will most likely occur.
- At 50 to 60 percent, CNS (central nervous system) manifestations become more pronounced. The patient will exhibit seizure activity. Abnormal pat-terns in respirations may be present. A comatose condition is expected at this level of carboxyhemoglobin. At 60 to 70 percent, onset of ventricular fibrillation (rapid, irregular heartbeat) and respiratory arrest is expected.
- At 70 percent, there is death.
Skin color
As the percentage of useful hemoglobin decreases, skin color goes from normal to pale to cyanotic (blue). What has so frequently been taught as an indication of carbon monoxide poisoning, that is, the cherry red coloring of the mucosa (mucous membrane), erythema (reddish colored rash) on the body, appears to be a finding very late in the progress of the poisoning.
While these have been noted in some cases relatively early in the poisoning process, the absence of these signs in no way rules out carbon monoxide poisoning. It is interesting to note that some symptoms, particularly CNS disorders, may not appear for up to three weeks after exposure It is for this reason that when confronted with a patient exhibiting CNS abnormalities a history must be taken. If the patient has no history of a CNS disturbance, no history of associated trauma (and in a child, no history of fever), questions should be aimed at exposure to carbon monoxide or other toxic agents.
Carbon monoxide poisoning and pregnancy
At special risk is the pregnant patient exposed to carbon monoxide. Studies have shown that carboxyhemoglobin levels in the baby are approximately twice that of the mother. Immediately after finishing one cigarette, carboxyhemoglobin levels of as high as 10 percent have been recorded. This would yield a fetal carboxyhemoglobin level of as much as 20 percent.
The health risks to the fetus of nine months of such exposure have been well documented. Also at special risk is the patient with chronic lung problems. This patient’s gas exchange mechanism is already compromised and the inhaletion of carbon monoxide only serves to compound the preexisting problem. Also at risk are children, due to their relatively high respiratory rate and their small volume of blood (and therefore hemoglobin).
Field Treatment of Carbon Monoxide Poisoning
Initial action when dealing with the suspected victim of carbon monoxide poisoning is aimed at removing him from the toxic environment. Needless to say, prior to removing a victim from an environment with a high carbon monoxide level, the rescuer should don SCBA (self-contained breathing apparatus). Filter masks are useless for carbon monoxide.
An important axiom to remember when rescuing a victim from a potentially hazardous environment: FIRST — PROTECT YOURSELF! Carboxyhemoglobin is eventually eliminated from the blood by the liver and the lungs. Field treatment is therefore directed at resolving acute problems and providing supportive therapy. In all cases where no other condition is present that would preclude it, the victim’s head should be elevated to reduce cerebral edema (swelling of the brain).
In the conscious patient, 100% oxygen should be administered by a mask with an attached oxygen reservoir. Hyperventilation should be encouraged. The patient’s clothing should be loosened and he should be kept warm. These steps will help the patient to most efficiently utilize the remaining unattached hemoglobin.
Reports of studies done at major trauma centers with decompression chambers extol the benefits of hyperbaric (high pressure) oxygen therapy when used on patients suffering from carbon monoxide poisoning. As with any unusual procedure, this too has its opponents. However, in the field, such a patient can never be given too much oxygen. Stimulants are contra indicated in the earlier stages of carbon monoxide poisoning. CPR should be maintained when indicated, with this patient the same as any patient with compromised cardiac activity.
Remember
Keep in mind during your patient assessment of a carbon monoxide victim rescued from a fire that the patient is also suffering from smoke in-halation. Evaluate and treat burns appropriately. Look for singed facial and nasal hairs. Noisy respirations or breath sounds may indicate the patient has inhaled fire gasses and suffered thermal burns of his airway.
Also observe the exhaled gasses for the presence of soot. Should any of these checks prove positive, the presence of bronchospasm, pulmonary edema and/ or laryngeal edema should be suspected.
Endotracheal intubation may be indicated rather early in the treatment of such patients to prevent airway obstruction caused by the edema. It is extremely important to summon emergency medical responders with advanced life support capabilities. In the smoke inhalation/carbon monoxide poisoning victim, narcotic analgesics should be withheld due to their respiratory depressant effects.
Conclusion
Colorless, odorless, tasteless, non-irritating; carbon monoxide is indeed a covert killer. It sneaks up on its victims, lulls them into a false sense of security, and kills them. Statistically, 62.4 percent of deaths in structure fires are due to the inhalation of smoke, carbon monoxide, etc. Obviously, the best treatment is prevention.
This article has been written by James H. Redford MD for Prepper’s Will.
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