Yes, many inhalers will leave levels of up to 34 percent alcohol in your lungs, although not absorbed into your blood stream you could still fail.
A breathalyzer or breathalyser (a portmanteau of breath and analyzer/analyser) is a device for estimating blood alcohol content (BAC) from a breath sample. Breathalyzer is the brand name of a series of models made by one manufacturer of breath alcohol testing instruments (originally Smith and Wesson, later sold to National Draeger), and is a registered trademark for such instruments. In Canada, a preliminary non-evidentiary screening device can be approved by Parliament as an approved screening device, and an evidentiary breath instrument can be similarly designated as an approved instrument. The U.S. National Highway Traffic Safety Administration maintains a Conforming Products List of breath alcohol devices approved for evidentiary use, as well as for preliminary screening use.
A 1927 paper produced by Emil Bogen, who collected air in a football bladder and then tested this air for traces of alcohol, discovered that the alcohol content of 2 litres of expired air was a little greater than that of 1 cc of urine. However, research into the possibilities of using breath to test for alcohol in a person's body dates as far back as 1874, when Anstie made the observation that small amounts of alcohol were excreted in breath.
Also, in 1927 a Chicago chemist, W.D. McNalley, invented a breathalizer in which the breath moving through chemicals in water would change color. One use for his invention was for house wives to test whether their husbands had been drinking before letting them in the house.
The first practical roadside breath-testing device intended for use by the police was the drunkometer. The drunkometer was developed by Professor Rolla N. Harger in 1938. The drunkometer collected a motorist's breath sample directly into a balloon inside the machine. The breath sample was then pumped through an acidified potassium permanganate solution. If there was alcohol in the breath sample, the solution changed colour. The greater the colour change, the more alcohol there was present in the breath.
In late 1927, in a case in Marlborough, England, a Dr. Gorsky, Police Surgeon, asked a suspect to inflate a football bladder with his breath. Since the 2 liters of the man's breath contained 1.5 ml of ethanol,] [ Dr. Gorsky testified before the court that the defendant was "50% drunk". Though technologies for detecting alcohol vary, it is widely accepted that Dr. Robert Borkenstein (1912–2002), a captain with the Indiana State Police and later a professor at Indiana University at Bloomington, is regarded as the first to create a device that measures a subject's blood alcohol level based on a breath sample. In 1954, Borkenstein invented his Breathalyzer, which used chemical oxidation and photometry to determine alcohol concentration. Subsequent breath analyzers have converted primarily to infrared spectroscopy. The invention of the Breathalyzer provided law enforcement with a non-invasive test providing immediate results to determine an individual's breath alcohol concentration at the time of testing. Also, the breath alcohol concentration test result itself can vary between individuals consuming identical amounts of alcohol due to gender, weight, and genetic pre-disposition.
It was in Britain, in 1967, that Tom Parry Jones developed and marketed the first electronic breathalyser. He established Lion Laboratories in Cardiff with his colleague, electrical engineer Bill Dulcie. The Road Safety Act 1967 introduced the first legally enforceable maximum blood alcohol level for drivers in the UK, above which it became an offence to be in charge of a motor vehicle; and introduced the roadside breathalyser, made available to police forces across the country. In 1979, Lion Laboratories' version of the breathalyser, known as the Alcolyser and incorporating crystal-filled tubes that changed colour above a certain level of alcohol in the breath, was approved for police use. Lion Laboratories won the Queen's Award for Technological Achievement for the product in 1980, and it began to be marketed worldwide. The Alcolyser was superseded by the Lion Intoximeter 3000 in 1983, and later by the Lion Alcolmeter and Lion Intoxilyser. These later models used a fuel cell alcohol sensor rather than crystals, providing a more reliable kerbside test and removing the need for blood or urine samples to be taken at a police station. In 1991, Lion Laboratories was sold to the American company MPD, Inc.
When the user exhales into a breath analyzer, any ethanol present in their breath is oxidized to acetic acid at the anode:
CH3CH2OH(g) + H2O(l) → CH3CO2H(l) + 4H+(aq) + 4e-
At the cathode, atmospheric oxygen is reduced:
O2(g) + 4H+(aq) + 4e- → 2H2O(l)
The overall reaction is the oxidation of ethanol to acetic acid and water.
CH3CH2OH(l) + O2(g) → CH3COOH(l) + H2O(l)
The electrical current produced by this reaction is measured by a microprocessor, and displayed as an approximation of overall blood alcohol content (BAC) by the Alcosensor.
People who have drunk alcohol will release special gases. It will approach silica gel of strong oxidizing agent K2Cr2O7. If the released gas contains ethanol (CH3CH2OH) steam, ethanol will be oxidized by chromium trioxide to form acetaldehyde. Meanwhile, CrO3 is restored as acetic acid [CH3COOH].
Breath analyzers do not directly measure blood alcohol content or concentration, which requires the analysis of a blood sample. Instead, they estimate BAC indirectly by measuring the amount of alcohol in one's breath. Two breathalyzer technologies are most prevalent. Desktop analyzers generally use infrared spectrophotometer technology, electrochemical fuel cell technology, or a combination of the two. Hand-held field testing devices are generally based on electrochemical platinum fuel cell analysis and, depending upon jurisdiction, may be used by officers in the field as a form of "field sobriety test" commonly called PBT (preliminary breath test) or PAS (preliminary alcohol screening) or as evidential devices in POA (point of arrest) testing.
There are many models of consumer or personal breath alcohol testers on the market. These devices are generally less expensive than the devices used by law enforcement. Most retail consumer breath testers use semiconductor-based sensing technology, which is less expensive, less accurate, and less reliable than fuel cell and infrared devices.
All breath alcohol testers sold to consumers in the United States are required to be certified by the Food and Drug Administration, while those used by law enforcement must be approved by the Department of Transportation's National Highway Traffic Safety Administration.
Manufacturers of over-the-counter consumer breath analyzers must submit an FDA 510(k) Premarket Clearance to demonstrate that the device to be marketed is at least as safe and effective, that is, substantially equivalent, to a legally marketed device (21 CFR 807.92(a) (3)) that is not subject to Premarket Approval (PMA). Submitters must compare their device to one or more similar legally marketed devices and make and support their substantial equivalency claims. The devices are cleared as "screeners" which means they have met the requirements used by the FDA for detecting the presence of alcohol in the breath. Screener certification does not mean that the device can measure breath alcohol content accurately. Many breath analyzers cleared by the FDA are very inaccurate when it comes to BAC measurement. No semiconductor device has ever been approved for evidential use (to stand-up in a court of law) by any State Law Enforcement Agencies or the U.S. Department of Transportation.
Public Breathalyzers are starting to become a popular method for consumers to test themselves at the source of alcohol consumption. They are now able to be found in almost any type of licensed business. Public Fuel Cell Breathalyzers are used in pubs, bars, restaurants, charities, weddings and all types of licensed events.Canadian Breath Analyzer Company manufactures and distributes fuel cell models for public and private consumer use. Canadian Breath Analyzer's unit utilizes an electrochemical fuel cell sensor which is the latest representation of public and mobile scanner technology. Fuel Cells are more expensive and also much more reliable than their semiconductor counterparts. CBA Company's unit is the CBA-FC-Multi. CBAC has also gone a few steps further and conducts educational seminars on breathalyzer technology. These units are tested by the R.C.M.P. and endorsed to be as accurate as their handheld, roadside scanners.
In France, possession of such a device is a legal obligation from 1 July 2012. All drivers of terrestrial motor vehicles (with the exception of mopeds) must be in possession of an unexpired device, and be able to show that it is immediately available for use. Drivers of vehicles that are equipped with an electronic immobilizer breathalyser are exempt from this requirement. Failure to carry a breathalyzer becomes a punishable offence from 1 November 2012. To be in compliance with this decree, the breathalyzer must conform to NF (NFX 20702).
The breath alcohol content reading is used in criminal prosecutions in two ways. The operator of a vehicle whose reading indicates a BAC over the legal limit for driving will be charged with having committed an per seillegal offense: that is, it is automatically illegal throughout the United States to drive a vehicle with a BrAC of 0.08 or higher. One exception is the state of Wisconsin, where a first time drunk driving offense is normally a civil ordinance violation. The uniformity is due to federal guidelines, since motor vehicle laws are states'; in earlier years the range of the threshold varied considerably between States. The breath analyzer reading will be offered as evidence of that crime, although the issue is what the BrAC was at the time of driving rather than at the time of the test. Some jurisdictions now allow the use of breath analyzer test results without regard as to how much time passed between operation of the vehicle and the time the test was administered.][ The suspect will also be charged with driving under the influence of alcohol (sometimes referred to as driving or operating while intoxicated). While BrAC tests are not necessary to prove a defendant was under the influence, laws in most states require the jury to presume that he was under the influence if his BrAC is found and believed to be over 0.08 (grams of alcohol/210 liters breath) when driving.][ This is a rebuttable presumption, however: the jury can disregard the test if they find it unreliable or if other evidence establishes a reasonable doubt.
Infrared instruments are also known as "evidentiary breath testers" and generally produce court-admissible results. Other instruments, usually hand held in design, are known as "preliminary breath testers" (PBT), and their results, while valuable to an officer attempting to establish probable cause for a drunk driving arrest, are generally not admissible in court. Some states, such as Idaho, permit data or "readings" from hand-held PBTs to be presented as evidence in court. If at all, they are generally only admissible to show the presence of alcohol or as a pass-fail field sobriety test to help determine probable cause to arrest. South Dakota does not permit data from any type of breath tester, and relies entirely on blood tests to ensure accuracy.
Breath testers can be very sensitive to temperature, for example, and will give false readings if not adjusted or recalibrated to account for ambient or surrounding air temperatures. The temperature of the subject is also very important.][
Breathing pattern can also significantly affect breath test results. One study found that the BAC readings of subjects decreased 11–14% after running up one flight of stairs and 22–25% after doing so twice][. Another study found a 15% decrease in BAC readings after vigorous exercise or hyperventilation][. Hyperventilation for 20 seconds has been shown to lower the reading by approximately 11%. On the other hand, holding one's breath for 30 seconds can increase the breath test result by about 16%.
Some breath analysis machines assume a hematocrit (cell volume of blood) of 47%][. However, hematocrit values range from 42 to 52% in men and from 37 to 47% in women. It has been theorized that a person with a lower hematocrit will have a falsely high BAC reading][.
Research indicates that breath tests can vary at least 15% from actual blood alcohol concentration][. An estimated 23% of individuals tested will have a BAC reading higher than their true BAC][. Police in Victoria, Australia, use breathalyzers that give a recognized 20% tolerance on readings. Noel Ashby, former Victoria Police Assistant Commissioner (Traffic & Transport), claims that this tolerance is to allow for different body types.
Many handheld breath analyzers sold to consumers use a silicon oxide sensor (also called a semiconductor sensor) to determine the blood alcohol concentration. These sensors are far more prone to contamination and interference from substances other than breath alcohol. The sensors require recalibration or replacement every six months. Higher end personal breath analyzers and professional-use breath alcohol testers use platinum fuel cell sensors. These too require recalibration but at less frequent intervals than semiconductor devices, usually once a year.
Calibration is the process of checking and adjusting the internal settings of a breath analyzer by comparing and adjusting its test results to a known alcohol standard. Law enforcement breath analyzers are meticulously maintained and re-calibrated frequently to ensure accuracy.
There are two methods of calibrating a precision fuel cell breath analyzer, the Wet Bath and the Dry Gas method. Each method requires specialized equipment and factory trained technicians. It is not a procedure that can be conducted by untrained users or without the proper equipment.
The Dry-Gas Method utilizes a portable calibration standard which is a precise mixture of alcohol and inert nitrogen available in a pressurized canister. Initial equipment costs are less than alternative methods and the steps required are fewer. The equipment is also portable allowing calibrations to be done when and where required.
The Wet Bath Method utilizes an alcohol/water standard in a precise specialized alcohol concentration, contained and delivered in specialized simulator equipment. Wet bath apparatus has a higher initial cost and is not intended to be portable. The standard must be fresh and replaced regularly.
Some semiconductor models are designed specifically to allow the sensor module to be replaced without the need to send the unit to a calibration lab.
One major problem with older breath analyzers is non-specificity: the machines not only identify the ethyl alcohol (or ethanol) found in alcoholic beverages, but also other substances similar in molecular structure or reactivity.
The oldest breath analyzer models pass breath through a solution of potassium dichromate, which oxidizes ethanol into acetic acid, changing color in the process. A monochromatic light beam is passed through this sample, and a detector records the change in intensity and, hence, the change in color, which is used to calculate the percent alcohol in the breath. However, since potassium dichromate is a strong oxidizer, numerous alcohol groups can be oxidized by it, producing false positives. This source of false positives is unlikely as very few other substances found in exhaled air are oxidizable.
Infrared-based breath analyzers project an infrared beam of radiation through the captured breath in the sample chamber and detect the absorbance of the compound as a function of the wavelength of the beam, producing an absorbance spectrum that can be used to identify the compound, as the absorbance is due to the harmonic vibration and stretching of specific bonds in the molecule at specific wavelengths (see infrared spectroscopy). The characteristic bond of alcohols in infrared is the O-H bond, which gives a strong absorbance at a short wavelength. The more light is absorbed by compounds containing the alcohol group, the less reaches the detector on the other side—and the higher the reading. Other groups, most notably aromatic rings and carboxylic acids can give similar absorbance readings.
Some natural and volatile interfering compounds do exist, however. For example, the National Highway Traffic Safety Administration (NHTSA) has found that dieters and diabetics may have acetone levels hundreds or even thousand of times higher than those in others. Acetone is one of the many substances that can be falsely identified as ethyl alcohol by some breath machines. However, fuel cell based systems are non-responsive to substances like acetone.
Substances in the environment can also lead to false BAC readings. For example, methyl tert-butyl ether (MTBE), a common gasoline additive, has been alleged anecdotally to cause false positives in persons exposed to it. Tests have shown this to be true for older machines; however, newer machines detect this interference and compensate for it. Any number of other products found in the environment or workplace can also cause erroneous BAC results. These include compounds found in lacquer, paint remover, celluloid, gasoline, and cleaning fluids, especially ethers, alcohols, and other volatile compounds.
Breath analyzers assume that the subject being tested has a 2100-to-1 partition ratio in converting alcohol measured in the breath to estimates of alcohol in the blood. If the instrument estimates the BAC, then it measures weight of alcohol to volume of breath, so it will effectively measure grams of alcohol per 2100 ml of breath given. This measure is in direct proportion to the amount of grams of alcohol to every 1 ml of blood. Therefore, there is a 2100-to-1 ratio of alcohol in blood to alcohol in breath. However, this assumed partition ratio varies from 1300:1 to 3100:1 or wider among individuals and within a given individual over time. Assuming a true (and US legal) blood-alcohol concentration of .07%, for example, a person with a partition ratio of 1500:1 would have a breath test reading of .10%—over the legal limit.
Most individuals do, in fact, have a 2100-to-1 partition ratio in accordance with William Henry's law, which states that when the water solution of a volatile compound is brought into equilibrium with air, there is a fixed ratio between the concentration of the compound in air and its concentration in water. This ratio is constant at a given temperature. The human body is 37 degrees Celsius on average. Breath leaves the mouth at a temperature of 34 degrees Celsius. Alcohol in the body obeys Henry's Law as it is a volatile compound and diffuses in body water. To ensure that variables such as fever and hypothermia could not be pointed out to influence the results in a way that was harmful to the accused, the instrument is calibrated at a ratio of 2100:1, underestimating by 9 percent. In order for a person running a fever to significantly overestimate, he would have to have a fever that would likely see the subject in the hospital rather than driving in the first place. Studies suggest that about 1.8% of the population have a partition ratio below 2100:1. Thus, a machine using a 2100-to-1 ratio could actually overestimate the BAC. As much as 14% of the population has a partition ratio above 2100, thus causing the machine to under-report the BAC. Further, the assumption that the test subject's partition ratio will be average—that there will be 2100 parts in the blood for every part in the breath—means that accurate analysis of a given individual's blood alcohol by measuring breath alcohol is difficult, as the ratio varies considerably.
Variance in how much one breathes out can also give false readings, usually low. This is due to biological variance in breath alcohol concentration as a function of the volume of air in the lungs, an example of a factor which interferes with the liquid-gas equilibrium assumed by the devices. The presence of volatile components is another example of this; mixtures of volatile compounds can be more volatile than their components, which can create artificially high levels of ethanol (or other) vapors relative to the normal biological blood/breath alcohol equilibrium.
One of the most common causes of falsely high breath analyzer readings is the existence of mouth alcohol. In analyzing a subject's breath sample, the breath analyzer's internal computer is making the assumption that the alcohol in the breath sample came from alveolar air—that is, air exhaled from deep within the lungs. However, alcohol may have come from the mouth, throat or stomach for a number of reasons.][ To help guard against mouth-alcohol contamination, certified breath-test operators are trained to observe a test subject carefully for at least 15–20 minutes before administering the test.
The problem with mouth alcohol being analyzed by the breath analyzer is that it was not absorbed through the stomach and intestines and passed through the blood to the lungs. In other words, the machine's computer is mistakenly applying the partition ratio (see above) and multiplying the result. Consequently, a very tiny amount of alcohol from the mouth, throat or stomach can have a significant impact on the breath-alcohol reading.
Other than recent drinking, the most common source of mouth alcohol is from belching or burping][. This causes the liquids and/or gases from the stomach—including any alcohol—to rise up into the soft tissue of the esophagus and oral cavity, where it will stay until it has dissipated. The American Medical Association concludes in its Manual for Chemical Tests for Intoxication (1959): "True reactions with alcohol in expired breath from sources other than the alveolar air (eructation, regurgitation, vomiting) will, of course, vitiate the breath alcohol results." For this reason, police officers are supposed to keep a DUI suspect under observation for at least 15 minutes prior to administering a breath test. Instruments such as the Intoxilyzer 5000 also feature a "slope" parameter. This parameter detects any decrease in alcohol concentration of 0.006 g per 210 L of breath in 0.6 second, a condition indicative of residual mouth alcohol, and will result in an "invalid sample" warning to the operator, notifying the operator of the presence of the residual mouth alcohol. PBT's, however, feature no such safeguard.
Acid reflux, or gastroesophageal reflux disease, can greatly exacerbate the mouth-alcohol problem. The stomach is normally separated from the throat by a valve, but when this valve becomes herniated, there is nothing to stop the liquid contents in the stomach from rising and permeating the esophagus and mouth. The contents—including any alcohol—are then later exhaled into the breathalyzer. Experiments on individuals suffering from this condition did not find any actual increase in Breath Ethanol.
Mouth alcohol can also be created in other ways. Dentures, some have theorized, will trap alcohol, although experiments have shown no difference if the normal 15 minute observation period is observed. Periodontal disease can also create pockets in the gums which will contain the alcohol for longer periods][. Also known to produce false results due to residual alcohol in the mouth is passionate kissing with an intoxicated person][. Recent use of mouthwash or breath fresheners can skew results upward as they can contain fairly high levels of alcohol][.
Absorption of alcohol continues for anywhere from 20 minutes (on an empty stomach) to two-and-one-half hours (on a full stomach) after the last consumption. Peak absorption generally occurs within an hour. During the initial absorptive phase, the distribution of alcohol throughout the body is not uniform. Uniformity of distribution, called equilibrium, occurs just as absorption completes. In other words, some parts of the body will have a higher blood alcohol content (BAC) than others. One aspect of the non-uniformity before absorption is complete is that the BAC in arterial blood will be higher than in venous blood. Other false positive of high BAC and also blood reading are related to Patients with proteinuria and hematuria, due to kidney metabolization and failure. The metabolization rate of related patients with kidney damage is abnormal in relation to percent in alcohol in the breath. However, since potassium dichromate is a strong oxidizer, numerous alcohol groups can be oxidized by kidney and blood filtration, producing false positives. .
During the initial absorption phase, arterial blood alcohol concentrations are higher than venous. After absorption, venous blood is higher. This is especially true with bolus dosing. With additional doses of alcohol, the body can reach a sustained equilibrium when absorption and elimination are proportional, calculating a general absorption rate of 0.02/drink and a general elimination rate of 0.015/hour. (One drink is equal to 1.5 ounces of liquor, 12 ounces of beer, or 5 ounces of wine.)
Breath alcohol is a representation of the equilibrium of alcohol concentration as the blood gases (alcohol) pass from the (arterial) blood into the lungs to be expired in the breath. Arterial blood distributes oxygen throughout the body. Breath alcohol concentrations are generally lower than blood alcohol concentrations, because a true representation of blood alcohol concentration is only possible if the lungs were able to completely deflate. Vitreous (eye) fluid provides the most accurate account of blood alcohol concentration][.
The breath analyzer test is usually administered at a police station, commonly an hour or more after the arrest. Although this gives the BrAC at the time of the test, it does not by itself answer the question of what it was at the time of driving. The prosecution typically provides an estimated alcohol concentration at the time of driving utilizing retrograde extrapolation, presented by expert opinion. This involves projecting back in time to estimate the BrAC level at the time of driving, by applying the physiological properties of absorption and elimination rates in the human body.][
Extrapolation is calculated using five factors and a general elimination rate of 0.015/hour.
For example: Time of breath test-10:00pm...Result of breath test-0.080...Time of driving-9:00pm (stopped by officer)...Time of last drink-8:00pm...Last food-12:00pm][
Using these facts, an expert can say the person's last drink was consumed on an empty stomach, which means absorption of the last drink (at 8:00) was complete within one hour-9:00. At the time of the stop, the driver is fully absorbed. The test result of 0.080 was at 10:00. So the one hour of elimination that has occurred since the stop is added in, making 0.080+0.015=0.095 the approximate breath alcohol concentration at the time of the stop.][
The photovoltaic assay, used only in the dated Photo Electric Intoximeter (PEI), is a form of breath testing rarely encountered today. The process works by using photocells to analyze the color change of a redox (oxidation-reduction) reaction. A breath sample is bubbled through an aqueous solution of sulfuric acid, potassium dichromate, and silver nitrate. The silver nitrate acts as a catalyst, allowing the alcohol to be oxidized at an appreciable rate. The requisite acidic condition needed for the reaction might also be provided by the sulfuric acid. In solution, ethanol reacts with the potassium dichromate, reducing the dichromate ion to the chromium (III) ion. This reduction results in a change of the solution's color from red-orange to green. The reacted solution is compared to a vial of non-reacted solution by a photocell, which creates an electric current proportional to the degree of the color change; this current moves the needle that indicates BAC.
Like other methods, breath testing devices using chemical analysis are somewhat prone to false readings. Compounds that have compositions similar to ethanol, for example, could also act as reducing agents, creating the necessary color change to indicate increased BAC.
There are a number of substances or techniques that can supposedly "fool" a breath analyzer (i.e., generate a lower blood alcohol content).
A 2003 episode of the popular science television show MythBusters tested a number of methods that supposedly allow a person to fool a breath analyzer test. The methods tested included breath mints, onions, denture cream, mouthwash, pennies and batteries; all of these methods proved ineffective. The show noted that using items such as breath mints, onions, denture cream and mouthwash to cover the smell of alcohol may fool a person, but, since they will not actually reduce a person's BAC, there will be no effect on a breath analyzer test regardless of the quantity used, if any, it appeared that using mouthwash only raised the BAC. Pennies supposedly produce a chemical reaction, while batteries supposedly create an electrical charge, yet neither of these methods affected the breath analyzer results.
The Mythbusters episode also pointed out another complication: It would be necessary to insert the item into one's mouth (e.g. eat an onion, rinse with mouthwash, conceal a battery), take the breath test, and then possibly remove the item — all of which would have to be accomplished discreetly enough to avoid alerting the police officers administering the test (who would obviously become very suspicious if they noticed that a person was inserting items into their mouth prior to taking a breath test). It would likely be very difficult, especially for someone in an intoxicated state, to be able to accomplish such a feat.
In addition, the show noted that breath tests are often verified with blood tests (which are more accurate) and that even if a person somehow managed to fool a breath test, a blood test would certainly confirm a person's guilt. However, it is not clear why a negative breath test would be verified by a subsequent blood test.
Other substances that might reduce the BAC reading include a bag of activated charcoal concealed in the mouth (to absorb alcohol vapor), an oxidizing gas (such as N2O, Cl2, O3, etc.) that would fool a fuel cell type detector, or an organic interferent to fool an infrared absorption detector. The infrared absorption detector is more vulnerable to interference than a laboratory instrument measuring a continuous absorption spectrum since it only makes measurements at particular discrete wavelengths. However, due to the fact that any interference can only cause higher absorption, not lower, the estimated blood alcohol content will be overestimated.][ Additionally, Cl2 is rather toxic and corrosive.
A 2007 episode of the Spike network's show Manswers showed some of the more common and not-so-common ways of attempts to beat the breath analyzer, none of which work. Test 1 was to suck on a copper-coated coin such as a penny. Test 2 was to hold a battery on the tongue. Test 3 was to chew gum. None of these tests showed a "pass" reading if the subject had consumed alcohol.
On the other hand, products such as mouthwash or breath spray can "fool" breath machines by significantly raising test results. Listerine mouthwash, for example, contains 27% alcohol. The breath machine is calibrated with the assumption that the alcohol is coming from alcohol in the blood diffusing into the lung rather than directly from the mouth, so it applies a partition ratio of 2100:1 in computing blood alcohol concentration—resulting in a false high test reading. To counter this, officers are not supposed to administer a PBT for 15 minutes after the subject eats, vomits, or puts anything in their mouth. In addition, most instruments require that the individual be tested twice at least two minutes apart. Mouthwash or other mouth alcohol will have somewhat dissipated after two minutes and cause the second reading to disagree with the first, requiring a retest. (Also see the discussion of the "slope parameter" of the Intoxilyzer 5000 in the "Mouth Alcohol" section above.)
This was clearly illustrated in a study conducted with Listerine mouthwash on a breath machine and reported in an article entitled "Field Sobriety Testing: Intoxilyzers and Listerine Antiseptic" published in the July 1985 issue of The Police Chief (p. 70). Seven individuals were tested at a police station, with readings of 0.00%. Each then rinsed his mouth with 20 milliliters of Listerine mouthwash for 30 seconds in accordance with directions on the label. All seven were then tested on the machine at intervals of one, three, five and ten minutes. The results indicated an average reading of 0.43 blood-alcohol concentration, indicating a level that, if accurate, approaches lethal proportions. After three minutes, the average level was still 0.020, despite the absence of any alcohol in the system. Even after five minutes, the average level was 0.011.
In another study, reported in 8(22) Drinking/Driving Law Letter 1, a scientist tested the effects of Binaca breath spray on an Intoxilyzer 5000. He performed 23 tests with subjects who sprayed their throats and obtained readings as high as 0.81—far beyond lethal levels. The scientist also noted that the effects of the spray did not fall below detectable levels until after 18 minutes.
Blood alcohol content
Asthma (from the Greek ἅσθμα, ásthma, "panting") is a common chronic inflammatory disease of the airways characterized by variable and recurring symptoms, reversible airflow obstruction, and bronchospasm. Common symptoms include wheezing, coughing, chest tightness, and shortness of breath.
Asthma is thought to be caused by a combination of genetic and environmental factors. Its diagnosis is usually based on the pattern of symptoms, response to therapy over time, and spirometry. It is clinically classified according to the frequency of symptoms, forced expiratory volume in one second (FEV1), and peak expiratory flow rate. Asthma may also be classified as atopic (extrinsic) or non-atopic (intrinsic) where atopy refers to a predisposition toward developing type 1 hypersensitivity reactions.
Treatment of acute symptoms is usually with an inhaled short-acting beta-2 agonist (such as salbutamol) and oral corticosteroids. In very severe cases, intravenous corticosteroids, magnesium sulfate, and hospitalization may be required. Symptoms can be prevented by avoiding triggers, such as allergens and irritants, and by the use of inhaled corticosteroids. Long-acting beta agonists (LABA) or leukotriene antagonists may be used in addition to inhaled corticosteroids if asthma symptoms remain uncontrolled. The prevalence of asthma has increased significantly since the 1970s. In 2011, 235–300 million people globally have been diagnosed with asthma, and it caused 250,000 deaths.
Asthma is characterized by recurrent episodes of wheezing, shortness of breath, chest tightness, and coughing. Sputum may be produced from the lung by coughing but is often hard to bring up. During recovery from an attack it may appear pus like due to high levels of white blood cells called eosinophils. Symptoms are usually worse at night and in the early morning or in response to exercise or cold air. Some people with asthma rarely experience symptoms, usually in response to triggers, whereas others may have marked and persistent symptoms.
A number of other health conditions occur more frequently in those with asthma, including gastro-esophageal reflux disease (GERD), rhinosinusitis, and obstructive sleep apnea. Psychological disorders are also more common, with anxiety disorders occurring in between 16–52% and mood disorders in 14–41%. However, it is not known if asthma causes psychological problems or if psychological problems lead to asthma.
Asthma is caused by a combination of complex and incompletely understood environmental and genetic interactions. These factors influence both its severity and its responsiveness to treatment. It is believed that the recent increased rates of asthma are due to changing epigenetics (heritable factors other than those related to the DNA sequence) and a changing living environment.
Many environmental factors have been associated with asthma's development and exacerbation including allergens, air pollution, and other environmental chemicals. Smoking during pregnancy and after delivery is associated with a greater risk of asthma-like symptoms. Low air quality from factors such as traffic pollution or high ozone levels, has been associated with both asthma development and increased asthma severity. Exposure to indoor volatile organic compounds may be a trigger for asthma; formaldehyde exposure, for example, has a positive association. Also, phthalates in PVC are associated with asthma in children and adults as are high levels of endotoxin exposure.
Asthma is associated with exposure to indoor allergens. Common indoor allergens include: dust mites, cockroaches, animal dander, and mold. Efforts to decrease dust mites have been found to be ineffective. Certain viral respiratory infections, such as respiratory syncytial virus and rhinovirus, may increase the risk of developing asthma when acquired as young children. Certain other infections, however, may decrease the risk.
The hygiene hypothesis is a theory which attempts to explain the increased rates of asthma worldwide as a direct and unintended result of reduced exposure, during childhood, to non-pathogenic bacteria and viruses. It has been proposed that the reduced exposure to bacteria and viruses is due, in part, to increased cleanliness and decreased family size in modern societies. Evidence supporting the hygiene hypothesis includes lower rates of asthma on farms and in households with pets.
Use of antibiotics in early life has been linked to the development of asthma. Also, delivery via caesarean section is associated with an increased risk (estimated at 20–80%) of asthma—this increased risk is attributed to the lack of healthy bacterial colonization that the newborn would have acquired from passage through the birth canal. There is a link between asthma and the degree of affluence.
Family history is a risk factor for asthma, with many different genes being implicated. If one identical twin is affected, the probability of the other having the disease is approximately 25%. By the end of 2005, 25 genes had been associated with asthma in six or more separate populations, including GSTM1, IL10, CTLA-4, SPINK5, LTC4S, IL4R and ADAM33, among others. Many of these genes are related to the immune system or modulating inflammation. Even among this list of genes supported by highly replicated studies, results have not been consistent among all populations tested. In 2006 over 100 genes were associated with asthma in one genetic association study alone; more continue to be found.
Some genetic variants may only cause asthma when they are combined with specific environmental exposures. An example is a specific single nucleotide polymorphism in the CD14 region and exposure to endotoxin (a bacterial product). Endotoxin exposure can come from several environmental sources including tobacco smoke, dogs, and farms. Risk for asthma, then, is determined by both a person's genetics and the level of endotoxin exposure.
A triad of atopic eczema, allergic rhinitis and asthma is called atopy. The strongest risk factor for developing asthma is a history of atopic disease; with asthma occurring at a much greater rate in those who have either eczema or hay fever. Asthma has been associated with Churg–Strauss syndrome, an autoimmune disease and vasculitis. Individuals with certain types of urticaria may also experience symptoms of asthma.
There is a correlation between obesity and the risk of asthma with both having increased in recent years. Several factors may be at play including decreased respiratory function due to a buildup of fat and the fact that adipose tissue leads to a pro-inflammatory state.
Beta blocker medications such as propranolol can trigger asthma in those who are susceptible. Cardioselective beta-blockers, however, appear safe in those with mild or moderate disease. Other medications that can cause problems are ASA, NSAIDs, and angiotensin-converting enzyme inhibitors.
Some individuals will have stable asthma for weeks or months and then suddenly develop an episode of acute asthma. Different individuals react differently to various factors. Most individuals can develop severe exacerbation from a number of triggering agents.
Home factors that can lead to exacerbation of asthma include dust, animal dander (especially cat and dog hair), cockroach allergens and mold. Perfumes are a common cause of acute attacks in women and children. Both viral and bacterial infections of the upper respiratory tract can worsen the disease. Psychological stress may worsen symptoms—it is thought that stress alters the immune system and thus increases the airway inflammatory response to allergens and irritants.
Asthma is the result of chronic inflammation of the airways which subsequently results in increased contractability of the surrounding smooth muscles. This among other factors leads to bouts of narrowing of the airway and the classic symptoms of wheezing. The narrowing is typically reversible with or without treatment. Occasionally the airways themselves change. Typical changes in the airways include an increase in eosinophils and thickening of the lamina reticularis. Chronically the airways' smooth muscle may increase in size along with an increase in the numbers of mucous glands. Other cell types involved include: T lymphocytes, macrophages, and neutrophils. There may also be involvement of other components of the immune system including: cytokines, chemokines, histamine, and leukotrienes among others.
While asthma is a well recognized condition, there is not one universal agreed upon definition. It is defined by the Global Initiative for Asthma as "a chronic inflammatory disorder of the airways in which many cells and cellular elements play a role. The chronic inflammation is associated with airway hyper-responsiveness that leads to recurrent episodes of wheezing, breathlessness, chest tightness and coughing particularly at night or in the early morning. These episodes are usually associated with widespread but variable airflow obstruction within the lung that is often reversible either spontaneously or with treatment".
There is currently no precise test with the diagnosis typically based on the pattern of symptoms and response to therapy over time. A diagnosis of asthma should be suspected if there is a history of: recurrent wheezing, coughing or difficulty breathing and these symptoms occur or worsen due to exercise, viral infections, allergens or air pollution. Spirometry is then used to confirm the diagnosis. In children under the age of six the diagnosis is more difficult as they are too young for spirometry.
Spirometry is recommended to aid in diagnosis and management. It is the single best test for asthma. If the FEV1 measured by this technique improves more than 12% following administration of a bronchodilator such as salbutamol, this is supportive of the diagnosis. It however may be normal in those with a history of mild asthma, not currently acting up. Single-breath diffusing capacity can help differentiate asthma from COPD. It is reasonable to perform spirometry every one or two years to follow how well a person's asthma is controlled.
The methacholine challenge involves the inhalation of increasing concentrations of a substance that causes airway narrowing in those predisposed. If negative it means that a person does not have asthma; if positive, however, it is not specific for the disease.
Other supportive evidence includes: a ≥20% difference in peak expiratory flow rate on at least three days in a week for at least two weeks, a ≥20% improvement of peak flow following treatment with either salbutamol, inhaled corticosteroids or prednisone, or a ≥20% decrease in peak flow following exposure to a trigger. Testing peak expiratory flow is more variable than spirometry, however, and thus not recommended for routine diagnosis. It may be useful for daily self-monitoring in those with moderate to severe disease and for checking the effectiveness of new medications. It may also be helpful in guiding treatment in those with acute exacerbations.
Asthma is clinically classified according to the frequency of symptoms, forced expiratory volume in one second (1FEV), and peak expiratory flow rate. Asthma may also be classified as atopic (extrinsic) or non-atopic (intrinsic), based on whether symptoms are precipitated by allergens (atopic) or not (non-atopic). While asthma is classified based on severity, at the moment there is no clear method for classifying different subgroups of asthma beyond this system. Finding ways to identify subgroups that respond well to different types of treatments is a current critical goal of asthma research.
Although asthma is a chronic obstructive condition, it is not considered as a part of chronic obstructive pulmonary disease as this term refers specifically to combinations of disease that are irreversible such as bronchiectasis, chronic bronchitis, and emphysema. Unlike these diseases, the airway obstruction in asthma is usually reversible; however, if left untreated, the chronic inflammation from asthma can lead the lungs to become irreversibly obstructed due to airway remodeling. In contrast to emphysema, asthma affects the bronchi, not the alveoli.
An acute asthma exacerbation is commonly referred to as an asthma attack. The classic symptoms are shortness of breath, wheezing, and chest tightness. While these are the primary symptoms of asthma, some people present primarily with coughing, and in severe cases, air motion may be significantly impaired such that no wheezing is heard.
Signs which occur during an asthma attack include the use of accessory muscles of respiration (sternocleidomastoid and scalene muscles of the neck), there may be a paradoxical pulse (a pulse that is weaker during inhalation and stronger during exhalation), and over-inflation of the chest. A blue color of the skin and nails may occur from lack of oxygen.
In a mild exacerbation the peak expiratory flow rate (PEFR) is ≥200 L/min or ≥50% of the predicted best. Moderate is defined as between 80 and 200 L/min or 25% and 50% of the predicted best while severe is defined as ≤ 80 L/min or ≤25% of the predicted best.
Acute severe asthma, previously known as status asthmaticus, is an acute exacerbation of asthma that does not respond to standard treatments of bronchodilators and corticosteroids. Half of cases are due to infections with others caused by allergen, air pollution, or insufficient or inappropriate medication use.
Brittle asthma is a kind of asthma distinguishable by recurrent, severe attacks. Type 1 brittle asthma is a disease with wide peak flow variability, despite intense medication. Type 2 brittle asthma is background well-controlled asthma with sudden severe exacerbations.
Exercise can trigger bronchoconstriction in both people with and without asthma. It occurs in most people with asthma and up to 20% of people without asthma. In athletes is diagnosed more commonly in elite athletes, with rates varying from 3% for bobsled racers to 50% for cycling and 60% for cross-country skiing. While it may occur with any weather conditions it is more common when it is dry and cold. Inhaled beta2-agonists do not appear to improve athletic performance among those without asthma however oral doses may improve endurance and strength.
Asthma as a result of (or worsened by) workplace exposures, is a commonly reported occupational disease. Many cases however are not reported or recognized as such. It is estimated that 5–25% of asthma cases in adults are work–related. A few hundred different agents have been implicated with the most common being: isocyanates, grain and wood dust, colophony, soldering flux, latex, animals, and aldehydes. The employment associated with the highest risk of problems include: those who spray paint, bakers and those who process food, nurses, chemical workers, those who work with animals, welders, hairdressers and timber workers.
Many other conditions can cause symptoms similar to those of asthma. In children, other upper airway diseases such as allergic rhinitis and sinusitis should be considered as well as other causes of airway obstruction including: foreign body aspiration, tracheal stenosis or laryngotracheomalacia, vascular rings, enlarged lymph nodes or neck masses. In adults, COPD, congestive heart failure, airway masses, as well as drug-induced coughing due to ACE inhibitors should be considered. In both populations vocal cord dysfunction may present similarly.
Chronic obstructive pulmonary disease can coexist with asthma and can occur as a complication of chronic asthma. After the age of 65 most people with obstructive airway disease will have asthma and COPD. In this setting, COPD can be differentiated by increased airway neutrophils, abnormally increased wall thickness, and increased smooth muscle in the bronchi. However, this level of investigation is not performed due to COPD and asthma sharing similar principles of management: corticosteroids, long acting beta agonists, and smoking cessation. It closely resembles asthma in symptoms, is correlated with more exposure to cigarette smoke, an older age, less symptom reversibility after bronchodilator administration, and decreased likelihood of family history of atopy.
The evidence for the effectiveness of measures to prevent the development of asthma is weak. Some show promise including: limiting smoke exposure both in utero and after delivery, breastfeeding, and increased exposure to daycare or large families but none are well supported enough to be recommended for this indication. Early pet exposure may be useful. Results from exposure to pets at other times are inconclusive and it is only recommended that pets be removed from the home if a person has allergic symptoms to said pet. Dietary restrictions during pregnancy or when breast feeding have not been found to be effective and thus are not recommended. Reducing or eliminating compounds known to sensitive people from the work place may be effective.
While there is no cure for asthma, symptoms can typically be improved. A specific, customized plan for proactively monitoring and managing symptoms should be created. This plan should include the reduction of exposure to allergens, testing to assess the severity of symptoms, and the usage of medications. The treatment plan should be written down and advise adjustments to treament according to changes in symptoms.
The most effective treatment for asthma is identifying triggers, such as cigarette smoke, pets, or aspirin, and eliminating exposure to them. If trigger avoidance is insufficient, the use of medication is recommended. Pharmaceutical drugs are selected based on, among other things, the severity of illness and the frequency of symptoms. Specific medications for asthma are broadly classified into fast-acting and long-acting categories.
Bronchodilators are recommended for short-term relief of symptoms. In those with occasional attacks, no other medication is needed. If mild persistent disease is present (more than two attacks a week), low-dose inhaled corticosteroids or alternatively, an oral leukotriene antagonist or a mast cell stabilizer is recommended. For those who have daily attacks, a higher dose of inhaled corticosteroids is used. In a moderate or severe exacerbation, oral corticosteroids are added to these treatments.
Avoidance of triggers is a key component of improving control and preventing attacks. The most common triggers include allergens, smoke (tobacco and other), air pollution, non selective beta-blockers, and sulfite-containing foods. Cigarette smoking and second-hand smoke (passive smoke) may reduce the effectiveness of medications such as corticosteroids. Dust mite control measures, including air filtration, chemicals to kill mites, vacuuming, mattress covers and others methods had no effect on asthma symptoms. Overall exercise, however is beneficial in people with stable asthma.
Medications used to treat asthma are divided into two general classes: quick-relief medications used to treat acute symptoms; and long-term control medications used to prevent further exacerbation.
Medications are typically provided as metered-dose inhalers (MDIs) in combination with an asthma spacer or as a dry powder inhaler. The spacer is a plastic cylinder that mixes the medication with air, making it easier to receive a full dose of the drug. A nebulizer may also be used. Nebulizers and spacers are equally effective in those with mild to moderate symptoms however insufficient evidence is available to determine whether or not a difference exists in those severe symptomatology.
Long-term use of inhaled corticosteroids at conventional doses carries a minor risk of adverse effects. Risks include the development of cataracts and a mild regression in stature.
When asthma is unresponsive to usual medications, other options are available for both emergency management and prevention of flareups. For emergency management other options include:
For those with severe persistent asthma not controlled by inhaled corticosteroids and LABAs bronchial thermoplasty may be an option. It involves the delivery of controlled thermal energy to the airway wall during a series of bronchoscopies. While it may increase exacerbation frequency in the first few months it appears to decrease the subsequent rate. Effects beyond one year are unknown. Evidence suggests that sublingual immunotherapy in those with both allergic rhinitis and asthma improve outcomes.
Many people with asthma, like those with other chronic disorders, use alternative treatments; surveys show that roughly 50% use some form of unconventional therapy. There is little data to support the effectiveness of most of these therapies. Evidence is insufficient to support the usage of Vitamin C. Acupuncture is not recommended for the treatment as there is insufficient evidence to support its use. Air ionisers show no evidence that they improve asthma symptoms or benefit lung function; this applied equally to positive and negative ion generators.
"Manual therapies", including osteopathic, chiropractic, physiotherapeutic and respiratory therapeutic maneuvers, have insufficient evidence to support their use in treating asthma. The Buteyko breathing technique for controlling hyperventilation may result in a reduction in medications use however does not have any effect on lung function. Thus an expert panel felt that evidence was insufficient to support its use.
The prognosis for asthma is generally good, especially for children with mild disease. Mortality has decreased over the last few decades due to better recognition and improvement in care. Globally it causes moderate or severe disability in 19.4 million people as of 2004 (16 million of which are in low and middle income countries). Of asthma diagnosed during childhood, half of cases will no longer carry the diagnosis after a decade. Airway remodeling is observed, but it is unknown whether these represent harmful or beneficial changes. Early treatment with corticosteroids seems to prevent or ameliorates a decline in lung function.
As of 2011, 235–330 million people worldwide are affected by asthma, and approximately 250,000 people die per year from the disease. Rates vary between countries with prevalences between 1 and 18%. It is more common in developed than developing countries. One thus sees lower rates in Asia, Eastern Europe and Africa. Within developed countries it is more common in those who are economically disadvantaged while in contrast in developing countries it is more common in the affluent. The reason for these differences is not well known. Low and middle income countries make up more than 80% of the mortality.
While asthma is twice as common in boys as girls, severe asthma occurs at equal rates. In contrast adult women have a higher rate of asthma than men and it is more common in the young than the old.
Global rates of asthma have increased significantly between the 1960s and 2008 with it being recognized as a major public health problem since the 1970s. Rates of asthma have plateaued in the developed world since the mid-1990s with recent increases primarily in the developing world. Asthma affects approximately 7% of the population of the United States and 5% of people in the United Kingdom. Canada, Australia and New Zealand have rates of about 14–15%.
Asthma was recognized in Ancient Egypt and was treated by drinking an incense mixture known as kyphi. It was officially named as a specific respiratory problem by Hippocrates circa 450 BC, with the Greek word for "panting" forming the basis of our modern name. In 200 BC it was believed to be at least partly related to the emotions.
In 1873, one of the first papers in modern medicine on the subject tried to explain the pathophysiology of the disease while one in 1872, concluded that asthma can be cured by rubbing the chest with chloroform liniment. Medical treatment in 1880, included the use of intravenous doses of a drug called pilocarpin. In 1886, F.H. Bosworth theorized a connection between asthma and hay fever. Epinephrine was first referred to in the treatment of asthma in 1905. Oral corticosteroids began to be used for this condition in the 1950s while inhaled corticosteroids and selective short acting beta agonist came into wide use in the 1960s.
During the 1930s–1950s, asthma was known as one of the "holy seven" psychosomatic illnesses. Its cause was considered to be psychological, with treatment often based on psychoanalysis and other talking cures. As these psychoanalysts interpreted the asthmatic wheeze as the suppressed cry of the child for its mother, they considered the treatment of depression to be especially important for individuals with asthma.
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Blood alcohol content (BAC), also called blood alcohol concentration, blood ethanol concentration, or blood alcohol level is most commonly used as a metric of alcohol intoxication for legal or medical purposes.
Blood alcohol content is usually expressed as a percentage of alcohol (generally in the sense of ethanol) in the blood. For instance, a BAC of 0.10 means that 0.10% (one tenth of one percent) of a person's blood, by volume (usually, but in some countries by mass), is alcohol.
In order to calculate estimated peak blood alcohol concentration (EBAC) a variation, including drinking period in hours, of the Widmark formula was used. The formula is:
where 0.806 is a constant for body water in the blood (mean 80.6%), SD is the number of standard drinks containing 10 grams of ethanol, 1.2 is a factor in order to convert the amount in grams to Swedish standards set by The Swedish National Institute of Public Health, BW is a body water constant (0.58 for men and 0.49 for women), Wt is body weight (kilogram), MR is the metabolism constant (0.017), DP is the drinking period in hours and 10 converts the result to permillage of alcohol. Regarding metabolism (MR) in the formula; Females demonstrated a higher average rate of elimination (mean, 0.017; range, 0.014-0.021 g/210 L) than males (mean, 0.015; range, 0.013-0.017 g/210 L). Female subjects on average had a higher percentage of body fat (mean, 26.0; range, 16.7-36.8%) than males (mean, 18.0; range, 10.2-25.3%). Additionally, men are, on average, heavier than women but it is not strictly accurate to say that the water content of a person alone is responsible for the dissolution of alcohol within the body, because alcohol does dissolve in fatty tissue as well. When it does, a certain amount of alcohol is temporarily taken out of the blood and briefly stored in the fat. For this reason, most calculations of alcohol to body mass simply use the weight of the individual, and not specifically his water content. Finally, it is speculated that the bubbles in sparkling wine may speed up alcohol intoxication by helping the alcohol to reach the bloodstream faster. A study conducted at the University of Surrey in the United Kingdom gave subjects equal amounts of flat and sparkling Champagne which contained the same levels of alcohol. After 5 minutes following consumption, the group that had the sparkling wine had 54 milligrams of alcohol in their blood while the group that had the same sparkling wine, only flat, had 39 milligrams.
In most jurisdictions a measurement such as a blood alcohol content (BAC) in excess of a specific threshold level, such as 0.05% or 0.08% defines the offense. Also, the National Institute on Alcohol Abuse and Alcoholism (NIAAA) define the term "binge drinking" as any time one reaches a peak BAC of 0.08% or higher as opposed to some (arguably) arbitrary number of drinks in an evening.
Known as pleasure zone, the positive effects exceed the negative at concentrations typically between 0.030–0.059% blood ethanol concentration (BEC), but the contrary becomes true at higher volumes (0.08% as defined by NIAAA); especially concentrations typical of binge drinking.
A BAC of 0.080 or more is considered "legally intoxicated" for driving in most American states. Likewise, ≤0.050 is considered NOT impaired in most states. In the State of Washington a driver can get charged with DUI (Revised Code of Washington 46.61.502 - Driving Under The Influence of Alcohol/Drugs) even if the person's BAC is under .08. The charge of DUI for anything under the .08 BAC threshold is based on whether or not the driver's ability to safely operate a motor vehicle is affected by alcohol, drugs or any combination thereof.
There are several different units in use around the world for defining blood alcohol concentration. Each is defined as either a mass of alcohol per volume of blood or a mass of alcohol per mass of blood (never a volume per volume). 1 milliliter of blood is approximately equivalent to 1.06 grams of blood. Because of this, units by volume are similar but not identical to units by mass. In the U.S. the concentration unit 1% w/v (percent mass/volume, equivalent to 10g/l or 1 g per 100 ml) is in use. This is not to be confused with the amount of alcohol measured on the breath, as with a breathalyzer. The amount of alcohol measured on the breath is generally accepted to be proportional to the amount of alcohol present in the blood at a rate of 1:2100. Therefore, a breathalyzer measurement of 0.10 mg/L of breath alcohol converts to 0.021 g/210L of breath alcohol, or 0.021 g/dL of blood alcohol (the units of the BAC in the United States). While a variety of units (or sometimes lack thereof) is used throughout the world, many countries use the g/L unit, which do not create confusion as percentages do. Usual units are highlighted in the table below.
For purposes of law enforcement, blood alcohol content is used to define intoxication and provides a rough measure of impairment. Although the degree of impairment may vary among individuals with the same blood alcohol content, it can be measured objectively and is therefore legally useful and difficult to contest in court. Most countries disallow operation of motor vehicles and heavy machinery above prescribed levels of blood alcohol content. Operation of boats and aircraft are also regulated.
The alcohol level at which a person is considered to be legally impaired varies by country. The list below gives limits by country. These are typically blood alcohol content limits for the operation of a vehicle.
It is illegal to have any measurable alcohol in the blood while driving in these countries. Most jurisdictions have a tolerance slightly higher than zero to account for false positives and naturally occurring alcohol in the body. Some of the following jurisdictions have a general prohibition of alcohol.
In certain countries, alcohol limits are determined by the Breath Alcohol Content (BrAC), not to be confused with blood alcohol content (BAC).
"0.01" Blood alcohol content is the hundredth decimal part of the one thousandth part of a liter. (Please note that this "0.01" is measured in permille and not percentage as the "0.1" example in introduction and numbers in 1 Effects at different levels.)
In digesting these numbers it must be remembered that one milliliter is the thousandth part of a liter. Therefore 1% of a milliliter is 0.00001-Liter. Expressing blood-alcohol concentration as "0.01" is naming the hundredth part of a thousandth part.
As final example, a blood-alcohol concentration of 0.08, being the 0.08 "part" of a milliliter (ITSELF the thousandth part of a Liter) therefore names an absolute blood-alcohol volume of 0.00008-Liter (within every liter of blood).
Each country or state may define BAC differently. For example, the state of California in the United States legally defines BAC as a ratio of grams of alcohol per 100 milliliters of blood, which is equal to grams of alcohol per deciliter of blood.
Since measurement must be accurate and inexpensive, several measurement techniques are used as proxies to approximate the true parts per million measure. Some of the most common are listed here: (1) Mass of alcohol per volume of exhaled breath (for example, 0.38 mg/L; see also breath gas analysis), (2) Mass per volume of blood in the body (for example, 0.08 g/dL), and (3) Mass of alcohol per mass of the body (for example, 0.0013 g/Kg).
The number of alcoholic beverages (drinks) consumed is often a poor measure of blood alcohol content because of variations in sex, body weight, and body fat.
An ethanol level of 0.10% is equal to 22 mmol/l or 100 mg/dl of blood alcohol. This same 0.10% BAC also equates to 0.10 g/dL of blood alcohol or 0.10 g/210L of exhaled breath alcohol or 0.476 mg/L of exhaled breath alcohol. Likewise, 0.10 mg/L of exhaled breath alcohol converts to 0.02% BAC, 0.022 g/dL of blood alcohol or 0.022 g/210L of exhaled breath alcohol.
Blood alcohol tests assume the individual being tested is average in various ways. For example, on average the ratio of blood alcohol content to breath alcohol content (the partition ratio) is 2100 to 1. In other words, there are 2100 parts of alcohol in the blood for every part in the breath. However, the actual ratio in any given individual can vary from 1300:1 to 3100:1, or even more widely. This ratio varies not only from person to person, but within one person from moment to moment. Thus a person with a true blood alcohol level of .08% but a partition ratio of 1700:1 at the time of testing would have a .10 reading on a Breathalyzer calibrated for the average 2100:1 ratio.
A similar assumption is made in urinalysis. When urine is analyzed for alcohol, the assumption is that there are 1.3 parts of alcohol in the urine for every 1 part in the blood, even though the actual ratio can vary greatly.
Breath alcohol testing further assumes that the test is post-absorptive—that is, that the absorption of alcohol in the subject's body is complete. If the subject is still actively absorbing alcohol, their body has not reached a state of equilibrium where the concentration of alcohol is uniform throughout the body. Most forensic alcohol experts reject test results during this period as the amounts of alcohol in the breath will not accurately reflect a true concentration in the blood.
Alcohol is absorbed throughout the gastrointestinal tract, but more slowly in the stomach than in the small or large intestine. For this reason, alcohol consumed with food is absorbed more slowly, because it spends a longer time in the stomach. Furthermore, alcohol dehydrogenase is present in the stomach lining. After absorption, the alcohol passes to the liver through the hepatic portal vein, where it undergoes a first pass of metabolism before entering the general bloodstream.
Alcohol is removed from the bloodstream by a combination of metabolism, excretion, and evaporation. The relative proportion disposed of in each way varies from person to person, but typically about 95% is metabolized by the liver. The remainder of the alcohol is eliminated through excretion in breath, urine, sweat, feces, milk and saliva. Excretion into urine typically begins after about 40 minutes, whereas metabolisation commences as soon as the alcohol is absorbed, and even before alcohol levels have risen in the brain.
Alcohol is metabolized mainly by the group of six enzymes collectively called alcohol dehydrogenase. These convert the ethanol into acetaldehyde (an intermediate that is actually more toxic than ethanol). The enzyme acetaldehyde dehydrogenase then converts the acetaldehyde into non-toxic Acetic acid.
Many physiologically active materials are removed from the bloodstream (whether by metabolism or excretion) at a rate proportional to the current concentration, so that they exhibit exponential decay with a characteristic halflife (see pharmacokinetics). This is not true for alcohol, however. Typical doses of alcohol actually saturate the enzymes' capacity, so that alcohol is removed from the bloodstream at an approximately constant rate. This rate varies considerably between individuals; Another sex based difference is in the elimination of alcohol. Persons below the age of 25][, women persons of certain ethnicities, and persons with liver disease may process alcohol more slowly, also false positive of High (BAC) reading are related to patients with proteinuria and hematuria, due to kidney-liver metabolism and failure. (for example, Hematuria 1+ protenuria 1+ ) Also have impaired acetaldehyde dehydrogenase; this causes acetaldehyde levels to peak higher, producing more severe hangovers and other effects such as flushing and tachycardia. Conversely, members of certain ethnicities that traditionally did not use alcoholic beverages have lower levels of alcohol dehydrogenases and thus "sober up" very slowly, but reach lower aldehyde concentrations and have milder hangovers. Rate of detoxification of alcohol can also be slowed by certain drugs which interfere with the action of alcohol dehydrogenases, notably aspirin, furfural (which may be found in fusel alcohol), fumes of certain solvents, many heavy metals, and some pyrazole compounds. Also suspected of having this effect are cimetidine (Tagamet), ranitidine (Zantac), and acetaminophen (Tylenol) (paracetamol).
Currently, the only known substance that can increase the rate of metabolism of alcohol is fructose. The effect can vary significantly from person to person, but a 100g dose of fructose has been shown to increase alcohol metabolism by an average of 80%. Fructose also increase false positive of High ratio (BAC) reading to Patients with proteinuria and hematuria, due to kidney-liver metabolism.
Alcohol absorption can be slowed by ingesting alcohol on a full stomach. Spreading the total absorption of alcohol over a greater period of time decreases the maximum alcohol level, decreasing the hangover effect. Thus, drinking on a full stomach or drinking while ingesting drugs which slow the breakdown of ethanol into acetaldehyde will reduce the maximum blood levels of this substance and thus decrease the hangover. Alcohol in non-carbonated beverages is absorbed more slowly than alcohol in carbonated drinks.
Retrograde extrapolation is the mathematical process by which someone's blood alcohol concentration at the time of driving is estimated by projecting backwards from a later chemical test. This involves estimating the absorption and elimination of alcohol in the interim between driving and testing. The rate of elimination in the average person is commonly estimated at .015 to .020 grams per deciliter per hour (g/dl/h), although again this can vary from person to person and in a given person from one moment to another. Metabolism can be affected by numerous factors, including such things as body temperature, the type of alcoholic beverage consumed, and the amount and type of food consumed.
In an increasing number of states, laws have been enacted to facilitate this speculative task: the blood alcohol content at the time of driving is legally presumed to be the same as when later tested. There are usually time limits put on this presumption, commonly two or three hours, and the defendant is permitted to offer evidence to rebut this presumption.
Forward extrapolation can also be attempted. If the amount of alcohol consumed is known, along with such variables as the weight and sex of the subject and period and rate of consumption, the blood alcohol level can be estimated by extrapolating forward. Although subject to the same infirmities as retrograde extrapolation—guessing based upon averages and unknown variables—this can be relevant in estimating BAC when driving and/or corroborating or contradicting the results of a later chemical test.
On Monday March 26, 2012, a man was found in a ditch in Indiana, USA with a BAC of 0.552%.
In November 2007, a driver was found passed out in her car in Oregon in the United States. A blood test showed her blood alcohol level was 0.550%. She was charged with several offenses, including two counts of driving under the influence of an intoxicant, reckless endangerment of a person, criminal mischief and driving with a suspended license. Her bail was later set at US$50,000, since she had several previous convictions for similar offenses.
In December 2007, a driver was arrested in Klamath County, Oregon, after she was found unconscious in her car which was stuck in a snow bank with its engine running. Police were forced to break a car window to remove her. After realizing she was in alcohol-induced coma, they rushed her to the hospital where a blood test showed her blood alcohol level was 0.720%. She reportedly was released from the hospital the next day. She was subsequently charged with drunk driving.
In July 2008, a driver was arrested after he ran into a highway message board on Interstate 95 in Providence, Rhode Island. A breath test showed his blood alcohol level was at 0.491% and he was raced to the hospital where he was sedated and placed in a detoxification unit. He was subsequently charged with driving while intoxicated and resisting arrest. He was later sentenced to one year probation, a $500 fine, 40 hours of community service and a one-year loss of his driver's license. The police later stated that his blood alcohol level was the highest they had ever seen for someone who hadn't died of alcohol poisoning. It was later estimated that the driver had consumed 10–14 drinks over the course of 1–2 hours, based on the standard levels of elimination which as documented previously can vary by up to 300%.
In December 2009, a South Dakota woman was found behind the wheel of a stolen car with a measured blood alcohol content of .708%, almost nine times the state's limit of .08%, thus becoming the highest recorded level of alcohol toxicity for the state. After she was hospitalized, she was released on bond and subsequently found in another stolen automobile while under the influence.
In August 2012, an Iowa man was arrested for driving under the influence. Breathalyzers and subsequent lab tests confirmed a BAC of .627%, over 8 times the legal limit for driving. At that blood alcohol level, he was conscious, yet incoherent and unable to answer simple questions.
There have been reported cases of blood alcohol content higher than 1.00%. In March 2009, a 45-year-old man was admitted to the hospital in Skierniewice, Poland, after being struck by a car. The blood test showed blood alcohol content at 1.23. The man survived but did not remember either the accident or the circumstances of his alcohol consumption. One such case was reported by O'Neil, and others in 1984. They report on a 30-year-old man who survived a blood alcohol concentration of 1,500 mg/100 ml blood after vigorous medical intervention.
In South Africa, a man driving a Mercedes-Benz Vito light van containing 15 sheep, allegedly stolen from nearby farms, was arrested on December 22, 2010, near Queenstown in Eastern Cape. His blood had an alcohol content of 1.6 g/100 ml. Also in the vehicle were five boys and a woman who were also arrested.
In 2004, an unidentified Taiwanese woman died of alcohol intoxication after immersion for twelve hours in a bathtub filled with 40% ethanol. Her blood alcohol content was 1.35%. It was believed that she had immersed herself as a response to the SARS epidemic.
In Poland, a homeless man was found sleeping half-naked on January 28, 2011, in Cieszyn. His blood had an alcohol level of 1.024%. Despite the temperature of −10 °C and extremely high blood alcohol content the man survived.
In December 2004, a man was admitted to the hospital in Plovdiv, Bulgaria, after being struck by a car. After detecting a strong alcohol odor, doctors at a hospital conducted a breath test which displayed the man's blood alcohol content at 0.914. The man was treated for serious injuries sustained in the crash and survived.
In February 2005, French gendarmes from Bourg-en-Bresse, France, conducted a breath test on a man who had lost control of his car. He had an alcohol content of 0.976. He was not injured in the accident but was charged with a €150 fine and his driving license was canceled.
In 1982, a 24-year-old woman was admitted to the UCLA emergency room with a serum alcohol concentration of 1.5 (1,510 mg/dL), corresponding to a BAC of 1.33. She was alert and oriented to person and place. Serum alcohol concentration is not equal to nor calculated in the same way as blood alcohol content.
In 2012, Oct 26th a man from Olszewo-Borki community, Poland, who died in a car accident, had 2.23%; however, the blood sample was collected from a wound and thus possibly contaminated.
Serotonergic: agonist35-HT responsible for GABAergic ( receptorAGABA PAM), glycinergic, and cholinergic (mAChR agonist) effects
Pneumoconiosis is an occupational lung disease and a restrictive lung disease caused by the inhalation of dust, often in mines.
Depending upon the type of dust, the disease is given different names:
Positive indications on patient assessment:
Pneumoconiosis in combination with multiple pulmonary rheumatoid nodules in rheumatoid arthritis patients is known as Caplan's syndrome.
Pneumoconiosis result in about 125,000 deaths a year as of 2010.
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An inhaler or puffer is a medical device used for delivering medication into the body via the lungs. It is mainly used in the treatment of asthma and Chronic Obstructive Pulmonary Disease (COPD). Zanamivir (Relenza), used to treat influenza, must be administered via inhaler. To reduce deposition in the mouth and throat, and to reduce the need for precise synchronization of the start of inhalation with actuation of the device, MDIs are sometimes used with a complementary spacer or holding chamber device.
MDI — The most common type of inhaler is the pressurized metered-dose inhaler (MDI). In MDIs, medication is most commonly stored in solution in a pressurized canister that contains a propellant, although it may also be a suspension. The MDI canister is attached to a plastic, hand-operated actuator. On activation, the metered-dose inhaler releases a fixed dose of medication in aerosol form. The correct procedure for using an MDI is to first fully exhale, place the mouth-piece of the device into the mouth, and having just started to inhale at a moderate rate, depress the canister to release the medicine. The aerosolized medication is drawn into the lungs by continuing to inhale deeply before holding the breath for 10 seconds to allow the aerosol to settle onto the walls of the bronchial and other airways of the lung.
DPI — Dry powder inhalers release a metered or device-measured dose of powdered medication that is inhaled through a DPI device.
Nebulizers — supply the medication as an aerosol created from an aqueous formulation.
In 1968, Robert Wexler of Abbott Laboratories developed the Analgizer, a disposable inhaler that allowed the self-administration of methoxyflurane vapor in air for analgesia. The Analgizer consisted of a polyethylene cylinder 5 inches long and 1 inch in diameter with a 1 inch long mouthpiece. The device contained a rolled wick of polypropylene felt which held 15 milliliters of methoxyflurane. Because of the simplicity of the Analgizer and the pharmacological characteristics of methoxyflurane, it was easy for patients to self-administer the drug and rapidly achieve a level of conscious analgesia which could be maintained and adjusted as necessary over a period of time lasting from a few minutes to several hours. The 15 milliliter supply of methoxyflurane would typically last for two to three hours, during which time the user would often be partly amnesic to the sense of pain; the device could be refilled if necessary. The Analgizer was found to be safe, effective, and simple to administer in obstetric patients during childbirth, as well as for patients with bone fractures and joint dislocations, and for dressing changes on burn patients. When used for labor analgesia, the Analgizer allows labor to progress normally and with no apparent adverse effect on Apgar scores. All vital signs remain normal in obstetric patients, newborns, and injured patients. The Analgizer was widely utilized for analgesia and sedation until the early 1970s, in a manner that foreshadowed the patient-controlled analgesia infusion pumps of today. The Analgizer inhaler was withdrawn in 1974, but use of methoxyflurane as a sedative and analgesic continues in Australia and New Zealand in the form of the Penthrox inhaler.
In 2009, the FDA banned the use of inhalers that utilize chlorofluorocarbons (CFC) as propellants for hydrofluorocarbons (HFA) inhalers; HFA is not environmentally inert as a greenhouse gas but does not affect the ozone layer. While some asthma sufferers and advocacy groups contend that the latter are not as effective, published clinical studies indicate equivalent control of asthma is achieved with use of HFA inhalers. Inhalers used to treat asthma contains dry powder spin inhalers and aerosoles containing suspending liquid medicament, but in both the cases the size of suspended particles or powder particles must be less than 5 micrometres so as to increase the surface area and deliver the drug to the inner most areas. Such a sufficiently small size of particles is necessary for dispersion and also for rapid action.
While the impact of CFC of inhalers on the ozone layer had been minuscule, the FDA in its interpretation of the Montreal Protocol mandated the switch in propellants. Patients expressed concern about the high price of the HFA inhalers as there is no generic version, which had been available in the CFC inhalers for many years. The elimination of generics from the market led to a price increase in inhalers that is expected to cost American consumers, insurances and the government about $8 billion by 2017.
The largest manufacturers of inhalers are GlaxoSmithKline (makers of the Advair Discus, a DPI), Merck, AstraZeneca (makers of Pulmicort and Symbicort) and Boehringer-Ingelheim (makers of Atrovent, Combivent, and Spiriva). BI, GSK, Merck, and AstraZeneca manufacture the medication being delivered via inhaler. However, 3M Drug Delivery Systems does some of the finished product manufacturing, as they are one of the leaders of MDI canisters, metering valves and other components.
Chronic obstructive pulmonary disease
Inhalation (also known as inspiration) is the flow of the respiratory current into an organism. In humans it is the movement of air from the external environment, through the airways, and into the alveoli.
Inhalation begins with the contraction of the muscles attached to the rib cage; this causes an expansion in the chest cavity. Then takes place the onset of contraction of the diaphragm, which results in expansion of the intrapleural space and an increase in negative pressure according to Boyle's Law. This negative pressure generates airflow because of the pressure difference between the atmosphere and alveolus. Air enters, inflating the lung through either the nose or the mouth into the pharynx (throat) and trachea before entering the alveoli.
Other muscles that can be involved in inhalation include:
Hyperaeration or hyperinflation is where the lung volume is abnormally increased, with increased filling of the alveoli. This results in an increased radiolucency on X-ray, a reduction in lung markings and depression of the diaphragm. It may occur in partial obstruction of a large airway, as in e.g. congenital lobar emphysema, bronchial atresia and mucous plugs in asthma.
It causes one form of overexpansion of the lung. Overexpansion, however, can also be caused by increase in lung mass itself.
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Chronic obstructive pulmonary disease (COPD), also known as chronic obstructive lung disease (COLD), chronic obstructive airway disease (COAD), chronic airflow limitation (CAL) and chronic obstructive respiratory disease (CORD), is a lung disease defined by persistently poor airflow as a result of breakdown of lung tissue (known as emphysema) and dysfunction of the small airways. It typically worsens over time. Primary symptoms include: shortness of breath, cough, and sputum production.
COPD is caused primarily by tobacco smoke, with a number of other factors playing a less common role. This triggers an inflammatory response in the lung. COPD is often defined based on low airflow on lung function tests. In contrast to asthma, this limitation is poorly reversible and usually gets increasingly worse over time.
Management involves quitting smoking, vaccinations, rehabilitation, and often inhaled bronchodilators. Some people may benefit from long-term oxygen therapy or lung transplantation.
Worldwide, COPD ranked as the sixth leading cause of death in 1990. Mortality is expected to increase due to an increase in smoking rates and an aging population in many countries. COPD is the third leading cause of death in the U.S., and the economic burden of COPD in the U.S. in 2007 was $42.6 billion in health care costs and lost productivity.
The most common symptoms of COPD are shortness of breath and a productive cough.
A chronic cough is usually the first symptom to occur. When it exists for more than three months a year for more than two years without another explanation, there is by definition chronic bronchitis. This condition can occur before COPD officially develops. The amount of sputum produced can can change over hours to days. In some cases the cough may not be present or only be occur occasionally and may not be productive. Some people with COPD write it off as simply a "smoker's cough". Sputum may be swallowed or spit out, depending often on social and cultural factors. Vigorous coughing may lead to rib fractures or a brief loss of consciousness. Those with COPD often have have a history of "common colds" that last a long time.
Shortness of breath is often the symptom that bother people the most. It commonly describe as: "my breathing requires effort," "I feel out of breath," or "I can't get enough air in". Different term; however may be used in different cultures. Typically the shortness of breath is of a prolonged duration, worsened over time and is worse with exercise. In the advanced stages it occurs during rest and maybe always present. It is a big reason for both anxiety and a poor quality of life in those with COPD.
Those with obstructed airflow may have wheezing or decreased sounds of air entry with poor air entry typically representing a greater severity of disease. It may also take longer to breath out than breathing in. Chest tightness may occur but is not common and may represent another problem. A barrel chest, while a classific finding, is also not a frequent finding. In those with severe disease tiredness and weight loss become common.
Advanced COPD may lead to cor pulmonale, a strain on the heart due to the extra work required to pump blood through the lungs. It is also the most common cause of the condition. Symptoms that indicate the presense of cor pulmonale include swelling of the ankles. Finger nail clubbing is not specific to COPD and should prompt investigations for an underlying lung cancer. Many people with COPD breath through pursed lips and this action can improve shortness of breath in some.
An exacerbation is defined as increased shortness of breath, increased sputum production, a change in the color of the sputum from clear to green or yellow, or an increase in cough in someone with COPD. This may present with signs of increased work of breathing such as: fast breathing, a fast heart rate, sweating, active use of muscles in the neck, a bluish tinge to the skin, and confusion if in a severe exacerbation.
COPD often occurs along with a number of other conditions due in part to common risk factors. These conditions include: ischemic heart disease, hypertension, diabetes mellitus, muscle wasting, osteoporosis, lung cancer, anxiety disorder and / or major depressive disorder.
Bronchial hyperresponsiveness, is a characteristic of asthma and refers to the increased sensitivity of the airways in response to an inhaled constrictor agonist. Many people with COPD also have this tendency. In COPD, the presence of bronchial hyperresponsiveness predicts a worse course of the disease.
The primary cause of COPD is tobacco smoke; with occupational exposures and pollution from indoor fires being a significant cause in some countries. Typically these exposures must occur over 10s of years before symptoms develop and genetics also affects the probability.
The primary risk factor for COPD globally is tobacco smoking. Other types of smoke are also a risk including: marijuana, cigar, second hand and water pipe smoke. In the United States, 80 to 90% of cases of COPD are due to smoking. Exposure to cigarette smoke is measured in pack-years, the average number of packages of cigarettes smoked daily multiplied by the number of years of smoking. The likelihood of developing COPD increases with age and cumulative smoke exposure, and almost all lifelong smokers will develop COPD, provided that smoking-related, extrapulmonary diseases (cardiovascular, diabetes, cancer) do not claim their lives beforehand.
In many developing countries, indoor air pollution from cooking fire smoke (often using biomass fuels such as wood and animal dung) is a common cause of COPD, especially in women. This is a common method of cooking and heating for nearly three billion people globally.
People who live in large cities have a higher rate of COPD compared to people who live in rural areas. While urban air pollution may be a contributing factor to exacervations its likely overall role in causing COPD is believed to be small.
Intense and prolonged exposure to workplace dusts found in coal mining, gold mining, and the cotton textile industry and chemicals such as cadmium, isocyanates, and fumes from welding have been implicated in the development of airflow obstruction, even in nonsmokers. Workers who smoke and are exposed to these particles and gases are even more likely to develop COPD. Intense silica dust exposure causes silicosis, a restrictive lung disease distinct from COPD; however, less intense silica dust exposures have been linked to a COPD-like condition. The effect of occupational pollutants on the lungs appears substantially less important than the effect of cigarette smoking. In the United States it is the cause of about 20% of cases overall and 30% of those in never-smokers. The rates are believed to be higher in the developing world.
Genetics play a role in the development of COPD. It is more common among relatives of those with COPD who smoke than unrelated smokers.
An inherited genetic condition, alpha 1-antitrypsin deficiency is responsible for about 2% of cases.
A number of other factors are less well linked to COPD. The risk is greater in those who are poor however it is no clear it this is due to poverty itself or other factors associated with poverty such as air pollution and nutrition. There is tentative evidence that those with asthma and airway hyperreactivity are at increased risk. Birth factors such as low birth weight may also play a role as do a number of infectious diseases including HIV/AIDS and tuberculosis.
An acute exacerbation of COPD is a sudden worsening of symptoms (shortness of breath, quantity and color of phlegm). It may be triggered by an infection or by environmental pollutants. Typically, infections cause 75% or more of the exacerbations; bacteria in 25% of cases, viruses in 25%, and both in 25%. Airway inflammation is increased during the exacerbation, resulting in increased hyperinflation, reduced expiratory air flow and worsening of gas transfer. This can also lead to hypoventilation and eventually hypoxia, insufficient tissue perfusion, and then cell necrosis. Pulmonary emboli can also worsening symptoms in those with COPD.
COPD is a type of obstructive lung disease in which chronic incompletely reversible airflow limit exists. This airflow limitation is due to break down of lung tissue (known as emphysema) and small airway disease known as obstructive bronchiolitis. The amount of these two factors vary between people. It developed secondary to an more pronounced and chronic inflammatory response to inhaled irritants. It is not fully understood how tobacco smoke and other inhaled particles damage the lungs to cause COPD. The most important processes causing lung damage are:
Narrowing of the airways reduces the airflow rate to and from the air sacs (alveoli) and limits effectiveness of the lungs. In COPD, the greatest reduction in air flow occurs when breathing out (during expiration) because the pressure in the chest tends to compress rather than expand the airways. In theory, air flow could be increased by breathing more forcefully, increasing the pressure in the chest during expiration. In COPD, there is often a limit to how much this can actually increase air flow, a situation known as expiratory flow limitation.
If the rate of airflow is too low, a person with COPD may not be able to completely finish breathing out (expiration) before he or she needs to take another breath. This is particularly common during exercise, when breathing must be faster. A little of the air of the previous breath remains within the lungs when the next breath is started, resulting in an increase in the volume of air in the lungs, a process called dynamic hyperinflation.
Dynamic hyperinflation is closely linked to shortness of breath in COPD. It is less comfortable to breathe with hyperinflation because it takes more effort to move the lungs and chest wall when they are already stretched by hyperinflation.
Another factor contributing to shortness of breath in COPD is the loss of the surface area available for the exchange of oxygen and carbon dioxide with emphysema. This reduces the rate of transfer of these gases between the body and the atmosphere and can lead to low oxygen and high carbon dioxide levels in the body. A person with emphysema may have to breathe faster or more deeply to compensate, which can be difficult to do if there is also flow limitation or hyperinflation.
Some people with advanced COPD do manage to breathe fast to compensate, but usually have shortness of breath as a result. Others, who may be less short of breath, tolerate low oxygen and high carbon dioxide levels in their bodies, but this can eventually lead to headaches, drowsiness and heart failure.
Advanced COPD can lead to complications beyond the lungs, such as weight loss (cachexia), pulmonary hypertension and right-sided heart failure (cor pulmonale). Osteoporosis, heart disease, muscle wasting and depression are all more common in people with COPD.
The diagnosis of COPD should be considered in anyone over the age of 35 to 40 who has shortness of breath, a chronic cough, sputum production, or frequent winter colds and a history of exposure to risk factors for the disease. Spirometry is then used to confirm the diagnosis; with an /FVC ratio1FEV of less than 0.7 following the use of a bronchodilator being diagnostic.
Spirometry measures the forced expiratory volume in one second (FEV1), which is the greatest volume of air that can be breathed out in the first second of a breath. Spirometry also measures the forced vital capacity (FVC), which is the greatest volume of air that can be breathed out in a whole large breath. Normally, at least 70% of the FVC comes out in the first second, giving a FEV1/FVC ratio of greater than 70%. A ratio of less than this defines as person as having COPD per the GOLD criteria. The NICE criteria additionally require a FEV1 of less than 80% of predicted.
According to the ERS criteria, it is FEV1% predicted that defines when a person has COPD, that is, when FEV1% predicted is < 88% for men, or < 89% for women. Evidence for using spirometry among those without symptoms in an effort to diagnose the condition earlier is of uncertain effect and therefore as of 2013 not recommended. A peak expiratory flow is not sufficient for the diagnosis.
A chest x-ray and complete blood count may be useful to exclude other conditions at the time of diagnosis. The classic signs of COPD on chest X-ray are over expanded lung, a flattened diaphragm, increased retrosternal airspace, and bulla while it can help exclude other lung diseases, such as pneumonia, pulmonary edema or a pneumothorax. Complete pulmonary function tests with measurements of lung volumes and gas transfer may also show hyperinflation and can discriminate between COPD with emphysema and COPD without emphysema. A high-resolution computed tomography scan of the chest may show the distribution of emphysema throughout the lungs and can also be useful to exclude other lung diseases.
An analysis of arterial blood is used to determine the need for oxygen. Testing is recommended in those with an FEV1 less than 35%, those with a peripheral oxygen saturation of less than 92% and those with congestive heart failure. In areas of the world were alpha-1 antitrypsin deficiency is common, people with COPD should be tested for it.
Axial CT image of the lung of a person with end-stage bullus emphysema.
A lateral chest x-ray of a person with emphysema. Note the barrel chest and flat diaphragm.
Lung bulla as seen on CXR in a person with severe COPD
A severe case of bullous emphysema
Spirometry can help to determine the severity of COPD. The FEV1 (measured after bronchodilator medication) is expressed as a percentage of a predicted "normal" value based on a person's age, gender, height and weight.
There are a number of methods to determine how much COPD is affecting a given individual. This depends partly on the severity of shortness of breath and exercise limitation. These and other factors can be combined with spirometry results to obtain a COPD severity score.
COPD Assessment Test (CAT) is a patient-completed questionnaire that assesses the impact of COPD (cough, sputum, dysnea, chest tighteness) on health status. The range of CAT scores is from 0–40. Higher the score, more the severity of the disease. The GOLD guidelines suggest dividing people into four categories based on current symptoms (assessed using the modified medical research council questionnaire or the CAT Score).
It is unclear if different types of COPD exist. While previously divided into emphysema and chronic bronchitis; emphysema is only a description of pathological lung changes rather than a disease in itself and is simply a descriptor of symptoms that may or may not occur with COPD.
Emphysema is an enlargement of the air spaces distal to the terminal bronchioles, with destruction of their walls. People with emphysema have historically been known as "Pink Puffers", due to their pink complexion.
Chronic bronchitis is defined in clinical terms as a cough with sputum production on most days for 3 months of a year, for 2 consecutive years. People with advanced COPD that have primarily chronic bronchitis were commonly referred to as "Blue Bloaters" because of the bluish color of the skin and lips (cyanosis) along with hypoxia and fluid retention.
COPD may need to be differentiated from congestive heart failure which often has jugular venous distension or pedal edema. If only one leg is swollen a deep vein thrombosis or pulmonary embolism should be considered. In those with poor air entry on one side versus both sides, pneumonia or pneumothorax may be the cause of shortness of breath. Many people with COPD mistakenly think they have asthma. The distinction between asthma and COPD however cannot be made via spirometry. Tuberculosis may also present with a chronic cough and should be considered in locations where it is common. Less common conditions which may present similarly include: bronchopulmonary dysplasia and obliterative bronchiolitis.
Annual influenza vaccinations and pneumococcal vaccinations may be beneficial.
Smoking cessation is one of the most important factors in slowing down the progression of COPD. Once COPD has been diagnosed, stopping smoking slows down the rate of progression of the disease. Even at a late stage of the disease, it can significantly reduce the rate of deterioration in lung function and delay the onset of disability and death. It is the only standard intervention that can improve the rate of progression of COPD.
Smoking cessation starts with an individual decision to stop smoking that leads to an attempt at quitting. Often several attempts are required before long-term smoking cessation is achieved. Some smokers can achieve long-term smoking cessation through willpower alone. However, smoking is highly addictive, and many smokers need further support to quit. The chance of successfully stopping smoking can be greatly improved through social support, engagement in a smoking cessation programme and the use of drugs such as nicotine replacement therapy, bupropion and varenicline.
The policies of governments, public health agencies and antismoking organizations can reduce smoking rates by encouraging stopping smoking and discouraging people from starting. These policies are important strategies in the prevention of COPD.][
Measures can be taken to reduce the likelihood that workers in at-risk industries—such as coal mining, construction and stonemasonry—will develop COPD. Examples of these measures include: education of workers and management about the risks, promoting smoking cessation, surveillance of workers for early signs of COPD, use of personal dust monitors, use of respirators, and dust control. Dust control can be achieved by improving ventilation, using water sprays and by using mining techniques that minimize dust generation. If a worker develops COPD, further lung damage can be reduced by avoiding ongoing dust exposure, for example by changing the work role.
Air quality can be improved by pollution reduction efforts, which should lead to health gains for people with COPD. A person who has COPD may experience fewer symptoms if they stay indoors on days when air quality is poor.
There is no known cure for COPD; however, it is both preventable and treatable. The major goals of management are to reduce risk factors, manage stable COPD, prevent and treat acute exacerbations and manage associated illnesses. The only measures that have been shown to reduce mortality is smoking cessation and supplemental oxygen. Stopping smoking decreases the risk of death by 18%. Other recommendations include: influenza vaccination once a year and reduction in exposure to environmental air pollution. Palliative care at the end of life may be useful, with morphine improving the feelings of shortness of breath. Additionally noninvasive ventilation may provide comfort.
Pulmonary rehabilitation is a program of exercise, disease management and counselling coordinated to benefit the individual. Pulmonary rehabilitation appears to improve over all quality of life, the ability to exercise, and mortality in those who have had a recent exacerbation. It has also been shown to improve the sense of control a patient has over their disease as well as their emotions. Breathing exercises in and of themselves appear to have a limited role.
Being either underweight or overweight can affect the symptoms, degree of disability and prognosis of COPD. People with COPD who are underweight can improve their breathing muscle strength by increasing their calorie intake. When combined with regular exercise or a pulmonary rehabilitation programme, this can lead to improvements in COPD symptoms. Supplemental nutrition may be useful in those who are malnourished.
Inhaled bronchodilators are the primary treatment. There are two major types, agonists2β and anticholinergics and they exist in long-acting and short-acting forms. They reduce shortness of breath, wheeze and exercise limitation, resulting in an improved quality of life. It is unclear if they change the progression of the underlying disease.
In those with mild disease short acting agents on an as needed basis are recommended. In those with more severe disease long acting agents and if not sufficient inhaled corticosteroids are recommended. With respect to long acting agents; it is unclear if tiotropium or long acting beta agonists (LABAs) are better and it may be worth trying each and continuing the one that worked best. Both types of agent reduce the risk of acute worsenings by 15-25%. While using both at the same time may offer a benefit, this benefit if any is of questionable significance.
There are several β2 agonists available including salbutamol (Ventolin) and terbutaline. They provide rapid relief of symptoms. Long acting β2 agonists such as salmeterol and formoterol are used as maintenance therapy and lead to improved airflow, exercise capacity, and quality of life. Long term use appears safe in COPD. Adverse effects include: shakiness and heart palpitations. When used with steroids they increase the risk of pneumonia.
There are two main anticholinergics used in COPD, ipratropium and tiotropium. Ipratropium is a short-acting agent while tiotropium is long acting one. Tiotropium is associated with a decrease in exacerbations and improved quality of life. While overall the two formulations do not appear to affect mortality; the dry powder form may decrease and the mist form may increase mortality. Anticholinergics can cause dry mouth and urinary tract symptoms. They are also associated with increase risk of heart disease and stroke.
Corticosteroids are usually used in inhaled form but may also be used as tablets to treat and prevent acute exacerbations. Well-inhaled corticosteroids (ICS) have not shown benefit for people with mild COPD, they decrease acute exacerbations in those with either moderate or severe disease. They however have no effect on overall one-year mortality and are associated with increased rates of pneumonia. It is unclear if the affect the progression of the disease.
Long term antibiotics specifically macrolides such as azithromycin reduce the frequency of exacerbations in those who have two or more a year. Methylxanthines such as theophylline generally causes more harm than benefit and thus are usually not recommended. It may be used as a second line agent in those not controlled by other measures.
Supplemental oxygen in those with low oxygen levels (a partial pressure of oxygen of less than 50 mmHg) decreases the risk of heart failure and death if used 15 hours per day. It may also improves peoples ability to exercise. In those with normal or mildly low oxygen levels, oxygen supplementation may improve shortness of breath. High concentrations of oxygen can lead to increased levels of carbon dioxide in some people with severe COPD. Smoking while on oxygen is a safety risk.
For those with very severe disease surgery is sometimes helpful and may include lung transplantation or lung volume reduction surgery. Lung volume reduction surgery involves removing the parts of the lung most damaged by emphysema allowing the remaining, relatively good lung to expand and work better. Lung transplantation is sometimes performed for severe COPD, particularly in younger individuals.
Acute exacerbations are typically treated by increases the usage of short acting bronchodilators. If this is not sufficient than oral corticosteroids may be useful. In those with a severe exacerbation antibiotics improve outcomes. There is no clear evidence for those with less severe cases. Non-invasive positive pressure ventilation in those with high CO2 levels decreases the probability of death or needing intubation. Additionally theophylline may have a role in those who do not respond to other measures.
COPD usually gradually gets worse over time and can ultimately result in death. It is estimated that 3% of all disability is related to COPD. The proportion of disability from COPD globally has decreased from 1990 to 2010 due to improved indoor air quality primarily in Asia. The overall number of years lived with disability from COPD; however, has increased. Results of spirometry is a good predictor of the future progress of the disease.
The rate at which it gets worse varies among individuals. The factors that predict a poorer prognosis are:
Prognosis in COPD can be estimated using the Bode Index. This scoring system uses FEV1, body-mass index, 6-minute walk distance, and the modified MRC dyspnea scale to estimate outcomes in COPD.
Globally as of 2010 COPD affected approximately 329 million people (4.8% of the population) and is slightly more common in men than women. This is as compared to 64 million being affected in 2004. The number of deaths from COPD has decreased slightly from 3.1 million to 2.9 million from 1990 to 2010. Overall it is the 4th leading cause of death. Rates are higher in older people with it occurs in 34-200 out of 1000 older than 65 years depending on the population looked at.
In the developing world the rates of COPD have increased significantly between the 1970s and the 2000s due in part to increasing rates of cigarette smoking in these regions of the world. In the developed world some countries have seen increased rates, some have remained stable and some have seen a lessening of COPD.
In England, an estimated 842,100 of 50 million people have a diagnosis of COPD; translating into approximately one person in 59 receiving a diagnosis of COPD at some point in their lives. In the most socioeconomically deprived parts of the country, one in 32 people were diagnosed with COPD, compared with one in 98 in the most affluent areas. In the United States, the prevalence of COPD is approximately 1 in 20 or 5%, totalling approximately 13.5 million people in USA, or possibly 25 million people if undiagnosed cases are included.
The term "emphysema" is derived from the Greek emphysan meaning "inflate" -itself composed of ἐν en, meaning "in", and φυσᾶν physan, meaning "breath, blast".
COPD has probably always existed but has been called by different names in the past. Bonet, in 1679, described a condition of "voluminous lungs". Giovanni Morgagni, in 1769, described 19 cases where the lungs were "turgid" particularly from air. The first description and illustration of the enlarged airspaces in emphysema was provided by Ruysh in 1721. Matthew Baillie illustrated an emphysematous lung in 1789 and described the destructive character of the condition. Badham used the word "catarrh" to describe the cough and mucus hypersecretion of chronic bronchitis in 1814. He recognised that chronic bronchitis was a disabling disorder.
René Laennec, the physician who invented the stethoscope, used the term "emphysema" in his book A Treatise on the Diseases of the Chest and of Mediate Auscultation (1837) to describe lungs that did not collapse when he opened the chest during an autopsy. He noted that they did not collapse as usual because they were full of air and the airways were filled with mucus.
In 1842, John Hutchinson invented the spirometer, which allowed the measurement of vital capacity of the lungs. However, his spirometer could only measure volume, not airflow. Tiffeneau in 1947 and Gaensler in 1950 and 1951 described the principles of measuring airflow.
The terms chronic bronchitis and emphysema were formally defined at the CIBA guest symposium of physicians in 1959. The term COPD was first used by William Briscoe in 1965 and has gradually overtaken other terms to become established today as the preferred name for this disease.
It is a challenge] Why?[ for many health systems to ensure appropriate identification, diagnosis and care for people with COPD; Britain's Department of Health has identified this as a major issue for the National Health Service and has introduced a specific strategy for COPD to tackle these problems.
In Europe COPD represents 3% of health care spending. In the United States costs of the disease are estimated at $50 billion most of which is due to exacerbation.
Infliximab has been tested in COPD but there was no evidence of benefit with the possibility of harm. Roflumilast shows promise in decreasing the rate of exacerbations but does not appear to change quality of life. A number of new long acting agents are under development.
Chronic obstructive pulmonary disease in horses also known as recurrent airway obstruction is an inflammatory disease of the airways due to an allergic reaction to straw containing fungus.
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A Respiratory Therapist is specialized healthcare practitioner who has graduated from a college or a university and passed a national board certifying examination. Respiratory therapists work under the general supervision of a primary provider, such as physician or nurse practitioner most often in intensive care and operating rooms, but also in outpatient clinics.
Respiratory therapists are specialists and educators in cardiology and pulmonology. Respiratory therapists are also advanced-practice clinicians in airway management; establishing and maintaining the airway during management of trauma, intensive care, and may administer anaesthesia for surgery or conscious sedation.
Driving under the influence (DUI), driving while intoxicated (DWI), drunk(en) driving, drink driving, drunk driving, operating under the influence, drinking and driving, or impaired driving is the crime of driving a motor vehicle with blood levels of alcohol in excess of a legal limit ("Blood Alcohol Content", or "BAC"). Similar regulations cover driving or operating certain types of machinery while affected by drinking alcohol or taking other drugs, including, but not limited to prescription drugs. This is a criminal offense in most nations. Convictions do not necessarily involve actual driving of the vehicle.
In most jurisdictions, a quantitative measurement such as a blood alcohol content (BAC) in excess of a specific threshold level, such as 0.05% or 0.08%, defines the offense with no need to prove impairment or intoxication. In some jurisdictions, there is an aggravated category of the offense at a higher BAC level, such as 0.12%. In most countries, anyone who is convicted of injuring or killing someone while under the influence of alcohol or drugs can be heavily fined, as in France, in addition to being given a lengthy prison sentence. Many employers or occupations have their own rules and BAC limits; for example, the United States Federal Railroad Administration has a 0.04% limit for train crew.[dead link] Certain large corporations have their own rules; for example, Union Pacific Railroad has their own BAC limit of 0.02% that, if violated during a random test or a for-cause test — for example, after a traffic accident — can result in termination of employment with no chance of future re-hire. Some jurisdictions have multiple levels of BAC for different categories of drivers; for example, the state of California has a general 0.08% BAC limit, a lower limit of 0.04% for commercial operators, and a limit of 0.01% for drivers who are under 21 or on probation for previous DUI offenses.
Alcohol laws are laws in relation to the manufacture, use, influence and sale of ethanol (ethyl alcohol, EtOH) or alcoholic beverages that contains ethanol.
Some countries forbid alcoholic beverages, or have forbidden them in the past. People trying to get around prohibition turn to smuggling of alcohol - known as bootlegging or rum-running - or make moonshine, a distilled beverage in an unlicensed still.
A metered-dose inhaler (MDI) is a device that delivers a specific amount of medication to the lungs, in the form of a short burst of aerosolized medicine that is usually self-administered by the patient via inhalation. It is the most commonly used delivery system for treating asthma, chronic obstructive pulmonary disease (COPD) and other respiratory diseases. The medication in a metered dose inhaler is most commonly a bronchodilator, corticosteroid or a combination of both for the treatment of asthma and COPD. Other medications less commonly used but also administered by MDI are mast cell stabilizers, such as cromoglicate or nedocromil.
A metered-dose inhaler consists of three major components; the canister which is produced in aluminium or stainless steel by means of deep drawing, where the formulation resides; the metering valve, which allows a metered quantity of the formulation to be dispensed with each actuation; and an actuator (or mouthpiece) which allows the patient to operate the device and directs the aerosol into the patient's lungs., The formulation itself is made up of the drug, a liquefied gas propellant and, in many cases, stabilising excipients. The actuator contains the mating discharge nozzle and generally includes a dust cap to prevent contamination.
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Dosage forms (also called unit doses) are essentially pharmaceutical products in the form in which they are marketed for use, typically involving a mixture of active drug components and nondrug components (excipients), along with other non-reusable material that may not be considered either ingredient or packaging (such as a capsule shell, for example). The term unit dose can also sometimes encompass non-reusable packaging as well (especially when each drug product is individually packaged), although the FDA distinguishes that by unit-dose "packaging" or "dispensing.". Depending on the context, multi(ple) unit dose can refer to distinct drug products packaged together, or to a single drug product containing multiple drugs and/or doses. The term dosage form can also sometimes refer only to the chemical formulation of a drug product's constituent drug substance(s) and any blends involved, without considering matters beyond that (like how it's ultimately configured as a consumable product such as a capsule, patch, etc.). Because of the somewhat vague boundaries and unclear overlap of these terms and certain variants and qualifiers thereof within the pharmaceutical industry, caution is often advisable when conversing outside of one's typical discourse community.
Depending on the method/route of administration, dosage forms come in several types. These include many kinds of liquid, solid, and semisolid dosage forms. Common dosage forms include pill, tablet, or capsule, drink or syrup, and natural or herbal form such as plant or food of sorts, among many others. Notably, the route of administration (ROA) for drug delivery is dependent on the dosage form of the substance in question. A liquid dosage form is the liquid form of a dose of a chemical compound used as a drug or medication intended for administration or consumption.