chronic and occult carbon monoxide poisoning: we don’t know what we’re missing - best liquid propane gas grills

by:Longzhao BBQ     2020-05-07
chronic and occult carbon monoxide poisoning: we don’t know what we’re missing  -  best liquid propane gas grills
Carbon monoxide has no color, no smell and is everywhere in our environment.
It is well known that it is an invisible killer at a large concentration.
This article reviews evidence that carbon monoxide is a public health threat even at much lower concentrations.
The hidden poisoning of carbon monoxide poisoning is a color-free, odor-free, non-irritant gas.
It naturally exists in our environment. 40%)
And artificial because of human activities (60%).
Large amounts of CO are released into the atmosphere by burning fossil fuels (
Forest fires, exhaust emissions from cars and burning natural gas).
9 people may have long-term contact with CO due to smoking or air pollution.
In addition, endogenous CO was also produced due to the decomposition of haem.
There are many other potential CO sources that are usually recorded in the poisoning report (table 1).
These sources are often associated with confined space.
They include incomplete combustion and insufficient ventilation of domestic natural gas, indoor combustion of charcoal for barbecue, propane gas cylinders (Forklift)
Alpha-chlorine exposure from gasoline generators and painting (
Liver conversion to CO).
11-15 View this table: See the inline View pop-up table 1 Why are the common causes of accidental CO poisoning missing carbon monoxide poisoning?
The medical literature is filled with dozens of case reports and commentary articles related to the insidious nature of this poison.
The editorial urges doctors to always be vigilant when looking for CO victims, but the diagnosis is still missing, which is not uncommon. Why is this?
It is rare for a doctor to make enough diagnosis to forget it.
Even in the face of classic symptoms (box 2)
There are signs of a long list of differential diagnosis.
Box 2 common symptoms caused by carbon monoxide poisoning dizziness, vomiting and conscious diarrhea (
No lateral signs)
To make a diagnosis, a blood test is performed and a joint diagnosis is obtained
For the measurement of carbon and oxygen hemoglobin (COHB)
This in itself is enough to discourage some clinicians.
Many people still think that an arterial sample is needed, and a venous sample is enough.
In dealing with the spectral part of low-level CO exposure, there is confusion about what poisoning is.
There are several reasons for this: due to the production of endogenous CO, we have some COHB in our blood.
10 Air pollution can increase COHB in a small amount in non-atmospheresmokers.
17, 18 smokers raised the level of COHB to between 5% and 9%, but the level of heavy smokers may be as high as 15%.
18, 19 in the indoor environment, smokers become net contributors to the CO level of the environment.
In any case, the correlation between COHB levels and symptoms is poor, especially in smokers with low atmospheric CO levels
Biochemical markers for 12A chronic CO poisoning have not yet been found.
There is relatively little research on this issue.
There is still debate about the mechanism of CO toxicity.
20 it was suggested that gas chromatography was required in order to accurately measure low levels of COHB.
Gas chromatography is relatively expensive and difficult to approach.
9 even in a controlled scientific environment, the dynamics of CO absorption and excretion are complex, and it is known that COHB in the blood reaches a stable state for more than eight hours of rest.
21 exercise reduces the time to reach a stable state, and breathing higher concentrations of CO in a balanced state produces higher concentrations of COHB.
22 COHB is reduced in air with a half-life of about 320 minutes.
However, if 100% of the oxygen is given to the patient, this half-life is further reduced to 80 minutes.
23 in the daily situation where a patient may smoke (or non-
Smokers who breathe air pollution
And then randomly leaving the potential CO source, one can only guess the actual dynamics of the person, especially when they receive oxygen on their way to the hospital.
The net effect of the above list is to leave the clinician (
Who thought of the possible diagnosis of CO poisoning)
There is a difficult question: "is the level of COHB in this person sufficient to lead to their clinical condition? If so, is exposure to CO acute or chronic, and what is the relevance of their smoking history?
"Is there any evidence at the moment that CO is a mysterious poison?
Descriptive patient study of chronic/recessive poisoning balzan et al measured COHB levels in 104 patients admitted to coronary artery care.
Of the 3 patients, 24 were identified as CO poisoning, and another 5 had evidence of minor contact.
In a later study, Balzan et al selected 307 patients admitted to the acute nervous system.
CO poisoning occurred in 3 patients (
From 29 patients with impaired consciousness and no signs of sideways).
In a similar study, hecklin et al. screened 168 consecutive acute nervous system injuries and found 5 cases of CO poisoning, of which 2 were from 43 patients with seizures.
They also looked into patients with headaches.
Out of a total of 140 headache patients, the COHB level was measured in 48 patients.
CO in 7 countries (
Greater than 10%)
, The prevalence of CO toxicity was given in 14 studies. 6%.
3 of the 7 CO poisoning patients complained about headaches for more than a week and 3 did not have headachessmokers.
During follow-up, it was found that all seven people had a cause of smoking except smoking.
After 27. 12 months, another study was conducted in the same group and found that 4 of the 10% patients had a COHB level greater than 146 (3%)with headache.
Among the study population, 89 people were contacted to complete the risk factor data.
Significant predictors of increased COHB levels were the number of smokers per day, the use of stoves for heating, and fellow residents with symptoms at the same time.
In the second year, they tried to use these predictors to validate a predictive model to identify CO poisoning in patients in the emergency department.
However, the model identified only three of the four patients with a COHB level greater than 10% (
A total of 61 patients tested).
29 in what appears to be the final publication of the series, they were confirmed for 753 cases of acute surgery, medicine, neurology, and only two minor cases of poisoning.
30 This suggests that extensive screening in the emergency department will be expensive and ineffective unless the screening tool is used quickly and cheaply.
Dolan et al. investigated flu patients who went to the emergency department. like symptoms.
COHB levels were measured in 55 patients with qualified symptoms.
13 patients (23. 6%)
The level of COHB is greater than 10%.
However, a total of 637 patients developed symptoms that allowed inclusion in the study (
A total of 3998 seen during study
We need to ask if there is some bias to rule out so many patients.
A study in 31 Burney obtained instructions for the incidence of symptoms in patients with CO poisoning, which described large-scale poisoning in a high school.
12 A total of 184 people were exposed to 500 ppm for 150 minutes before the staff received the alarm (
COHB levels up to 30% in these tests).
The three most common symptoms are headaches (90%), dizziness (82%)And weaknesses (53%).
Smokers have the same time of symptoms as non-smokers
Once the toxic level is close, smokers.
But they don't think it's until they return to normal.
Citing the author, although the elimination rate of CO is the same, smokers are more tolerant of low levels of CO than non-smokerssmokers”.
Symptoms related to CO poisoning, such as headache, weakness, dizziness, poor exercise tolerance, etc. , are often encountered by general practitioners, and are also seen in the emergency department.
How many patients with chronic CO poisoning and this symptom are correctly diagnosed?
This is a difficult question to answer.
There is evidence that at least some people have been left out --
Webb and vaitkeficius published a case report for a 73-year-old woman who had been investigated for more than four months and had various neurological symptoms before making a correct diagnosis, 32 and Myers et al described the history of 8 cases of chronic CO exposure, lasting from three to three years.
Month population studiesIn 1969, Cohen et al. published a paper showing an increase in the mortality rate between myocardial infarction and an increase in time for environmental pollution and carbon monoxide in Los Angeles.
33 Kurt et al. subsequently studied the frequency of acute CPR complaints associated with ambient CO levels
They found a low but statistically significant association level between acute heart and lung disease and ambient CO levels.
The problem of population research is ecological fallacy. in ecological fallacy, some trends people see are not necessarily the result of research factors.
34 in this case, a good example is other contaminants rather than causing symptoms together.
However, Kurt et al found no association between the environmental level of other atmospheric pollutants and heart and lung diseases.
In a study involving seven major cities in the United States, environmental CO levels were associated with hospital admissions for heart failure, with a relative admission risk of 1. 1 to 1.
37 when associated with an increase in concentration of 10ppm CO.
Between 35. 1979 and 1988, Cobb and eszer studied all CO-related accidental deaths in the United States.
36. The author believes that the number of unintentional deaths decreased year-on-year, from 1513 in 1979 to 878 in 1988, mainly due to the reduction of CO emissions from new car exhaust since 1968 by more than 90%.
Of course, these deaths can be attributed to acute poisoning.
However, the authors continue to comment that the actual death toll associated with CO may be much higher than they reported, as common CO levels in urban outdoor air may induce arrhythmia to be uneven, people with heart disease will die suddenly.
They suggest "small changes in the level of the environment [of CO]
May lead to significant changes in the heart rate of susceptible populations ", and commented that the death rate due to coronary heart disease in the United States began to decline in 1968, at the same time, due to the Clean Air Act, total CO production fell by 30%.
In the UK, nearly 7 million tons of carbon dioxide are emitted into the atmosphere every year, 87% of which come from gasoline engines.
38 This is consistent with the increase in traffic, an increase of 50% over the value of 1970.
However, vehicle emissions have declined since 1990, probably because of the increasing use of catalytic converters in cars.
Expert Group on air quality standards (EPAQS)
The British Minister for Environmental Affairs was established in 1991.
The group made suggestions on air quality standards, taking into account the best evidence of the impact of contaminants on human health.
They recommend the environmental, transportation and regional departments (DETR)
Air quality standards for 10 ppm CO, measured by an average of 8 hours of operation.
The reason behind this is that this level of exposure will keep the COHB level at non-Smokers under 2 years old
5%, lower than the level of patients with known symptoms of coronary heart disease.
It is unlikely that ordinary smokers will be affected by this situation alone, as their COHB levels are already higher than they can achieve by breathing this air.
Will occasionally exceed the EPAQS standard
But few, for example, in the eight UK cities throughout 1992, the average number of each city is less than one day when the recommendation criteria are exceeded.
38 therefore, the environmental level of CO in the atmosphere may have little or no effect on the British population --
Except in rare cases.
Unfortunately, things don't seem so simple.
Evidence also from the United States suggests that levels of 10 ppm CO or below still have an impact on cardiovascular problems and the rate of admission to heart failure.
40 these 40 may have three reasons: first, the level of the environmental monitor does not reflect the personal exposure well.
It is best to consider the level of increase (
But apparently still relatively low)
At the monitoring station, individuals are more likely to be exposed to increased levels, exceeding the EPAQS standard.
Secondly, people with heart disease (
Especially heart failure)
May be particularly sensitive to CO
Third, the presence of other pressure sources, such as low temperatures, may alter the effect of CO.
One thing seems certain.
It is necessary to conduct independent, UK-based studies on the impact of environmental levels of CO on hospital stay and mortality, no matter how low their levels are.
Patient Group study with COHB levels greater than 10%
The severity and duration of existing heart disease increased, and the risk of myocardial infarction increased if the level increased to more than 15%.
If the patient has an acute myocardial infarction, the threshold for ventricular fibrillation can be reduced to 9% COHB.
41 patients with severe chronic bronchitis or swelling of air when breathing air after exposure to CO42, walking distance was significantly shortened, and in patients with low levels of COHB, intermittent lameness
41 The COHB concentration was only 4 even in normal subjects.
It has been shown that 4% limits working capacity and maximum oxygen consumption.
The potential of COSome people to as shows that CO itself can produce.
Smith and Steichen, however, reviewed all available epidemiology and animal studies in 1993.
They reviewed 41 studies in total and their conclusion was that CO was not heat-causing.
Of the 44 patients with acute poisoning, 30% or more may have delayed neuropsychiatric symptoms.
Forty-five symptoms include cognitive and personality changes, dementia, mental illness, Parkinson's disease, amnesia, depression, and incontinence.
There is also good evidence that significantly mild low levels of acute and chronic exposure can lead to varying degrees of neuropsychological impairment.
It is assumed that CO causes lipid peroxide in nerve tissue.
47 early hyperbaric oxygen therapy reduces the level of lipid peroxide, which will explain a decrease in the incidence of neurological sequelae after hyperbaric oxygen therapy.
The areas most often involved in the brain include white balls and deep white matter.
48A nerve psychological screening battery (CONSB)
Methods for evaluating CO neurotoxicity have been designed, 49 but this is of no practical use in predicting poisoning cases in the emergency department.
At present, there are various domestic CO detectors on the market.
There are three main types of 50: Bionic (Chem-
Optical battery technology)
These sensors try to chemically simulate the effect of CO on hemoglobin.
The gel-coated disk is discolored and darkened in the presence of CO.
The sensor then identifies the color changes and settings of the sound alarm.
This detector is cheap and requires very little power, so it can be powered by a battery.
In the presence of common household gases, they do not alarm in error, but the alarm is triggered by high and low temperatures or humidity.
Low levels of CO can be detected, but the problem with some of these devices is the low reset capability of the sensor.
The sensor reset may take 48 hours, during which a cumulative reading may trigger a false alarm.
Metal oxide semiconductors, the oldest sensor device in China, have produced and sold millions of units.
The heated sulfur dioxide reacts with CO.
Because tin needs to be heated over and over again, a lot of energy is needed, so these detectors use mains insertion devices.
The advantage is no need to check the battery.
The detector responds quickly to rising CO levels.
However, false alarms are very common due to cross-sensitivity with other household gases.
Over time, it is possible to lose sensitivity to CO and calibration drift.
Metal Oxide Semiconductor devices cannot detect CO levels below 100 ppm, so there is no benefit for detecting chronic exposure at a low level.
For 20 years, chemical and electro-chemical devices have been used in industrial detectors.
They are used more frequently in household detectors.
The three platinum electrodes are immersed in the electrolyte solution and react with CO to produce a small current.
These devices are battery powered, or have a built-in power supply and have sound alarms and LCD displays with memory capabilities.
These detectors can detect low levels of CO, which is very accurate initially.
They tend to be expensive and are susceptible to contamination and calibration drift over time.
False positives can be caused by the radiation.
A major drawback is that the life of the equipment may be only two years.
Many detector devices in the market, in the presence of dangerous levels of CO, will produce serious false alarm problems and life-threatening failures.
Manufacturers and government agencies around the world are still working to develop the ideal equipment, which will increase resistance to false positives and false negatives, improve accuracy, and improve the reliability and repeatability of alarms.
However, there is no doubt that life will continue to be lost, and there will be a large number of people who have long been exposed to low-level CO, unless the number of CO detectors installed in British homes has increased dramatically.
Expired breathing carbon monoxide measuring instrument simple and cheap expired breathing CO measuring equipment is now on the market (
For example, piCO and ToxCO cigarette kits from Rochester Bedfont Technology Co. , Ltd. , Kent, UK).
These devices are easy to calibrate and take only a few seconds to use.
Although general practitioners still use these tools primarily to assess smokers who are trying to give up their habits, they are excellent tools for the emergency department to diagnose CO poisoning.
The instrument is compact in structure, easy to carry and verified.
5 1,52 summary there is sufficient evidence that quite a few of our population are poisoned by high concentrations of CO
Among other healthy people, mysterious indoor exposure can lead to common symptoms such as headache, dizziness, weakness and difficulty in concentration.
People with pre-
Pollution alone can lead to an increase in morbidity and mortality. even in non-
Smokers exposed to ambient CO levels below the 10 ppm EPAQS standard averaged 8 hours.
In order to ensure that the current EPAQS standards are not exceeded in the future, constant monitoring will be required and independent public health studies will be required to see if standards should be lowered.
At present, the best way to identify victims of CO poisoning seems to be to raise the vigilance and awareness of medical practitioners.
Neuropsychological Test (
CONSB, for example)
It has been shown to be useful in the assessment of the nervous system of recognized poisoning, but in the emergency department it seems unlikely that these tools will develop into a common diagnostic tool.
Biochemical markers for chronic CO poisoning still need to be identified, but recent studies have shown that CO is also a physiological Messenger similar to no.
This has increased interest in CO at biochemical levels, and it is hoped that one of the results of this study will be the identification of this marker.
So what is the information to take home for busy emergency department staff?
Consultants and managers should encourage the use of domestic CO alarms as "blanket covers" for the entire population ".
Although the efficiency of this additional step needs to be evaluated, it should be possible to incorporate the use of the smoke generator into the triage process.
The ideal triage device will be based on the same principle as the blood oxygen meter.
The device does not need to measure the absorption intensity of two different wavelengths of light to indicate the relative content of oxygen hemoglobin and oxygen hemoglobin, but must take into account the additional dimensions of oxygen hemoglobin.
In fact, it will be a portable "carbon meter" placed on your finger ".
At present, this kind of equipment is not available commercially.
Otherwise, in the current situation, doctors and triage nurses need to be aware that patients with low levels of CO poisoning may go to the department on a regular basis.
Certain symptoms and clinical conditions should be used as a trigger alert for further investigation (
A typical example is a former healthy student living in a rented house, who recently had a headache, just the beginning of winter).
If there is no expired breath detector, the easiest option is to measure the venous sample of the COHB concentration.
In cases where COHB levels are within acceptable normal limits, but where chronic CO poisoning is still strongly suspected, patients should be encouraged to check any household gas appliances urgently.
The whole theme of CO poisoning epidemiology is shrouded in a gray fog.
There is no reliable blood test for screening, such as the diagnosis of diabetes or hypothyroidism.
We don't know what we're missing until such a simple investigation.
Memory, giore A, member of Kelly.
Chronic carbon monoxide exposure: clinical syndrome detected by a neuropsychological test.
J Clin Psychol1998; 54:555–67.
Road to OpenUrlCrossRefPubMedWeb Science, Naumova EA.
Hospitalized for carbon monoxide and heart failure: evidence of increased effects at low temperatures.
Outlook for Environmental Health106:649–53.
TL, Mogielnicki RP, Chandler, from OpenUrlPubMedWeb Science gallery Kurt.
Frequency of acute heart and lung discomfort is associated with ambient carbon monoxide levels. Chest1978; 74:10–14.
W, Jenson BL, Omaye ST, by openurlcrossrefpmedweb Science, Yang.
Environmental levels of inpatient and carbon monoxide for cardiovascular disease.
Environmental sanitation; 55:185–96.
Henry Jia, openurlcrosspubmedweb of science.
Carbon monoxide: not gone, not forgotten.
J. Emerg Med1999 Accid; 16:91–2.
Roy B. Crawford R.
Traps in diagnosis and management of carbon monoxide poisoning.
J. Emerg Med1996 Accid; 13:62–3.
OpenUrlAbstract/free full text TextMoore ME, Finestone AJ.
Case of headache disappearing.
Engel J Med1968; 1216.
Pearhopkinson JM, Pierce Pu, Oliver JS.
Carbon monoxide poisoning similar to stomach troubleBMJ1980; 281:214–15.
DK, Mahoney JJ, Stevenson.
Carbon monoxide and carbon-oxygen hemoglobinAdv pediatric 1995; 42:303–25.
OpenUrlPubMed radio frequency.
Carbon monoxide is produced.
Engel J Med1970; 282:207–9.
Varon J. garsman JD.
Revenge of the barbecue grill: carbon monoxide poisoning. West J Med1990; 153:656–7.
OpenUrlPubMedWeb of the Science Museum.
Large-scale carbon monoxide poisoning: clinical effects and treatment outcomes of 184 victims.
Ann emmerg Mede 1982; 11:394–9.
Meters of OpenUrlCrossRefPubMedWeb ScienceWharton, Bistowish JM, Hutchinson RH, etc.
Fatal carbon monoxide poisoning at the hotelJAMA1989; 261:1177–8.
Openurlcross EW medely EW, Moorehead B, Haponik, EF.
Headache of warehouse workers: Emergency assessment and management of 30 patients with carbon monoxide poisoning. Am J Med1995; 98:145–55.
SM of OpenUrlCrossRefPubMedWeb Science Holdings Silvers, Ms. Hampson NB.
Entertainment boat carbon monoxide poisoning. JAMA1995; 274:1614–16.
Rice of OpenUrlCrossRefPubMedWeb Science, galahmi, Trier, J.
The relationship between venous and arterial hemoglobin levels in patients with suspected carbon monoxide poisoning.
Ann emmerg Mede 1995; 25:481–3.
Open urlcrossrefpubmedweb Science road Stewart, baritard, Platt LR, etc.
C-hemoglobin levels in American blood donorsJAMA1974; 229:1187–95.
A, Uusitalo AJ, of OpenUrlCrossRefPubMedWeb Science Limited Seppanen.
Oxygen hemoglobin saturation associated with smoking and various occupational conditions.
Ann Clin Res1977; 9:261–8.
Scientific OpenUrlPubMedWeb rusrussel MAH.
Changes in blood carbon and oxygen hemoglobin during smoking.
J1973 graduate medicine; 49:684–7.
Turner M Hamilton, Hamilton-OpenUrlAbstract/free full text
Mr. Clark RJ.
Carbon monoxide poisoning: update. BMJ1999; 16:92–6.
OpenUrl Lawther PJ.
Carbon monoxide. In Br Bull1973; 31:256–60.
Stewart RD, Stewart RS, Stamm W, etc.
A quick estimate of the level of carbon-oxygen hemoglobin for firefighters. JAMA1976; 235:390–2.
Parkinson's disease in OpenUrlCrossRefPubMedWeb Science marks.
Carbon monoxide poisoning
First aid doctor 1990; 2:11–16.
Alimbalzan MV, Cacciottolo JM, Mifsud S.
Unstable sore throat and exposure to carbon monoxide.
J1994 graduate medicine; 70:699–702.
OpenUrlAbstract/free full Text audio Balzan MV, Agius, Debono shares.
Carbon monoxide poisoning: easy to treat but difficult to identify.
J1996 graduate medicine; 72:470–3.
OpenUrlAbstract/free full Text Heckerling PS, Leikin JB, Terzian CG, etc.
Hidden carbon monoxide poisoning in patients with acute nervous system disease.
Ten point data Toxicol1990; 28:29–44.
OpenUrl Heckerling PS.
Hidden carbon monoxide poisoning: the cause of headache in winter.
Am J. medg Med1987; 5:201–4.
PS, Leikin JB, Maturen A, etc. of OpenUrlCrossRefPubMedWeb Science GmbH Heckerling.
Predictors of hidden carbon monoxide poisoning in headache and dizziness patients.
An intern Med1987; 107:174–6.
Shopheckerling PS, Leikin JB, Maturen.
Hidden carbon monoxide poisoning: validation of predictive models. Am J Med1988; 84:251–6.
PS, Leikin JB, Maturen A, of OpenUrlCrossRefPubMedWeb Science consulting Heckerling.
Screening of hidden carbon monoxide poisoning patients admitted to the emergency department.
M. J. medg. Med1990; 8:301–4.
MC, Haltom TL, pig growth hormone and so on of openurlcross refpmedweb Science solar Dolan.
Levels of hemoglobin in influenza patientslike symptoms.
Ann emmerg Mede 1987; 16:782–6.
CJ, vaitkeficus PV of OpenUrlCrossRefPubMedWeb Science GmbH Webb.
Seasonal dementia due to carbon monoxide poisoning.
J Am Geriatr Soc1997; 45:1281–2.
Science's OpenUrlPubMedWeb cohen West, Dean M, Goldsmith
Survival of carbon monoxide and myocardial infarction
Arch Environ Health1969; 19:510–17.
Scientific openurlcrosspubmedweb. Robinson WS.
Ecological Association and individual behavior.
View of American sociology15:351–7.
Morris Road, Nau Mova en, RL on the River monasine.
Seven major cities in the United States are hospitalized for environmental air pollution and heart failure.
Public Health Association; 85:1363–65.
Cobb of Openel RA.
Unintentional carbon monoxide
In the United States, as of 1988, the number of deaths was 1979. JAMA1991; 266:659–63.
Science's openurlcrosspubmedweb Baker atkins well, Baker EL.
Occupational exposure leads to deterioration of coronary artery disease: a report and literature review of the deaths of both.
This is J Ind Med1985; 7:73–9.
Scientific OpenUrlPubMedWeb seatseaton PA, Agius R, Baxter PJ, etc.
Recommended carbon monoxide air quality standards.
London: Department of Environment, Transport and Regional, 1998.
Yang w, janisen BL, Omaye Street.
Environmental levels of inpatient and carbon monoxide for cardiovascular disease.
Environmental sanitation; 55:185–96.
Morris Road in Naumova EN.
Hospitalized for carbon monoxide and heart failure: evidence of increased effects at low temperatures.
Outlook for Environmental Health106:649–53.
Goldman Sachs BG.
Develop effective strategies for carbon monoxide poisoning.
1987 emergency medical report; 8:193–200.
PMA radio Calverley, legit Swie, Flenley DC.
Carbon monoxide and exercise tolerance in chronic bronchitis and swelling. BMJ1981; 283:876–80.
OpenUrlFREE full text horhorhorvath SM, Raven PB, Dahms TE, etc.
Maximum aerobic capacity at different levels of carbon hemoglobin.
J Appl Physiol1975; 38:300–2.
OpenUrlAbstract/free full Text copy Smith CJ, Stoken TJ.
Thermal potential of carbon monoxide.
Atheroscleros1993; 99:137–49.
A, Zibrak JD of OpenUrlCrossRefPubMedWeb Science archiernst.
Carbon monoxide poisoning
Engel J. Med1998; 339:1603–8.
Y, Zlotogorski, Z, Goran-Katzav V, etc. Arch Neurol1998; 55:845–8.
Openurlcross Web Science advanced.
Carbon monoxide-
The effect of brain lipid peroxide and oxygen therapy mediated.
Application of J Physiol1990; 68:997–1003.
OpenUrlAbstract/free full text zagzagami AS, les Lane AK, Merrick R.
Delayed deterioration of nervous system after carbon monoxide poisoning: MRI manifestations. J Neurol1993; 240:113–16.
LD, Myers RA, of OpenUrlCrossRefPubMedWeb Science GmbH Messier.
Neuropsychology screening battery for carbon monoxide emergency assessment
Poisoned Patient
J Clin Psychol1991; 47:675–84.
Scientific OpenUrlPubMedWeb Phillips working group.
Carbon monoxide detectors: you need to know.
Journal of Mass Science 1998; Jan:76–8.
Stewart RD, manager, RS, stammwa, etc.
A quick estimate of the levels of carbon-oxygen hemoglobin in firefighters. JAMA1976; 235:390–2.
Kurt TL Anderson RJ Reid WG
Rapid estimation of carbon-oxygen hemoglobin by breath sampling in an emergency.
Veterinary Toxicol1990 buzzing; 32:227–9.
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