What is COPD?
COPD, or chronic obstructive pulmonary (PULL-mun-ary) disease, is a progressive disease that makes it hard to breathe. “Progressive” means the disease gets worse over time.
COPD can cause coughing that produces large amounts of mucus (a slimy substance), wheezing, shortness of breath, chest tightness, and other symptoms.
Cigarette smoking is the leading cause of COPD. Most people who have COPD smoke or used to smoke. Long-term exposure to other lung irritants, such as air pollution, chemical fumes, or dust, also may contribute to COPD.
Overview
To understand COPD, it helps to understand how the lungs work. The air that you breathe goes down your windpipe into tubes in your lungs called bronchial tubes, or airways.
The airways are shaped like an upside-down tree with many branches. At the end of the branches are tiny air sacs called alveoli (al-VEE-uhl-eye).
The airways and air sacs are elastic. When you breathe in, each air sac fills up with air like a small balloon. When you breathe out, the air sac deflates and the air goes out.
In COPD, less air flows in and out of the airways because of one or more of the following:
The airways and air sacs lose their elastic quality.
The walls between many of the air sacs are destroyed.
The walls of the airways become thick and inflamed (swollen).
The airways make more mucus than usual, which tends to clog the airways.
In the United States, the term “COPD” includes two main conditions—emphysema (em-fi-SE-ma) and chronic obstructive bronchitis (bron-KI-tis).
In emphysema, the walls between many of the air sacs are damaged, causing them to lose their shape and become floppy. This damage also can destroy the walls of the air sacs, leading to fewer and larger air sacs instead of many tiny ones.
In chronic obstructive bronchitis, the lining of the airways is constantly irritated and inflamed. This causes the lining to thicken. Lots of thick mucus forms in the airways, making it hard to breathe.
Most people who have COPD have both emphysema and chronic obstructive bronchitis. Thus, the general term “COPD” is more accurate.
Outlook
COPD is a major cause of disability, and it’s the fourth leading cause of death in the United States. More than 12 million people are currently diagnosed with COPD. An additional 12 million likely have the disease and don’t even know it.
COPD develops slowly. Symptoms often worsen over time and can limit your ability to do routine activities. Severe COPD may prevent you from doing even basic activities like walking, cooking, or taking care of yourself.
Most of the time, COPD is diagnosed in middle-aged or older people. The disease isn’t passed from person to person—you can’t catch it from someone else.
COPD has no cure yet, and doctors don’t know how to reverse the damage to the airways and lungs. However, treatments and lifestyle changes can help you feel better, stay more active, and slow the progress of the disease.
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Chronic obstructive pulmonary disease
Chronic obstructive pulmonary disease (COPD) refers to chronic bronchitis and emphysema, a pair of two commonly co-existing diseases of the lungs in which the airways become narrowed. This leads to a limitation of the flow of air to and from the lungs causing shortness of breath. In contrast to asthma, the limitation of airflow is poorly reversible and usually gets progressively worse over time.
COPD is caused by noxious particles or gas, most commonly from tobacco smoking, which triggers an abnormal inflammatory response in the lung. The inflammatory response in the larger airways is known as chronic bronchitis, which is diagnosed clinically when people regularly cough up sputum. In the alveoli, the inflammatory response causes destruction of the tissues of the lung, a process known as emphysema. The natural course of COPD is characterized by occasional sudden worsenings of symptoms called acute exacerbations, most of which are caused by infections or air pollution.
The diagnosis of COPD requires lung function tests. Important management strategies are smoking cessation, vaccinations, rehabilitation, and drug therapy (often using inhalers). Some patients go on to requiring long-term oxygen therapy or lung transplantation.
Worldwide, COPD ranked sixth as the cause of death in 1990. It is projected to be the third leading cause of death worldwide by 2020 due to an increase in smoking rates and demographic changes in many countries. COPD is the 4th 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.
COPD is also known as chronic obstructive lung disease (COLD), chronic obstructive airway disease (COAD), chronic airflow limitation (CAL) and chronic obstructive respiratory disease (CORD).
Signs and symptoms
One of the most common symptoms of COPD is shortness of breath (dyspnea). People with COPD commonly describe this as: “My breathing requires effort,” “I feel out of breath,” or “I can’t get enough air in”. People with COPD typically first notice dyspnea during vigorous exercise when the demands on the lungs are greatest. Over the years, dyspnea tends to get gradually worse so that it can occur during milder, everyday activities such as housework. In the advanced stages of COPD, dyspnea can become so bad that it occurs during rest and is constantly present.
Other symptoms of COPD are a persistent cough, sputum or mucus production, wheezing, chest tightness, and tiredness.
People with advanced (very severe) COPD sometimes develop respiratory failure. When this happens, cyanosis, a bluish discoloration of the lips caused by a lack of oxygen in the blood, can occur. An excess of carbon dioxide in the blood can cause headaches, drowsiness or twitching (asterixis). A complication of advanced COPD is cor pulmonale, a strain on the heart due to the extra work required by the heart to pump blood through the affected lungs. Symptoms of cor pulmonale are peripheral edema, seen as swelling of the ankles, and dyspnea.
There are a few signs of COPD that a healthcare worker may detect although they can be seen in other diseases. Some people have COPD and have none of these signs. Common signs are:
tachypnea, a rapid breathing rate
wheezing sounds or crackles in the lungs heard through a stethoscope
breathing out taking a longer time than breathing in
enlargement of the chest, particularly the front-to-back distance (hyperinflation)
active use of muscles in the neck to help with breathing
breathing through pursed lips
increased anteroposterior to lateral ratio of the chest (i.e. barrel chest).
Etiology
Smoking
The primary risk factor for COPD is chronic tobacco smoking. 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. Not all smokers will develop COPD, but continuous smokers have at least a 25% risk after 25 years. The likelihood of developing COPD increases with increasing age as the cumulative smoke exposure increases.
Occupational exposures
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 to be substantially less important than the effect of cigarette smoking.
Air pollution
Studies in many countries have found that people who live in large cities have a higher rate of COPD compared to people who live in rural areas. Urban air pollution may be a contributing factor for COPD as it is thought to slow the normal growth of the lungs although the long-term research needed to confirm the link has not been done. 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.
Genetics
Some factor in addition to heavy smoke exposure is required for a person to develop COPD. This factor is probably a genetic susceptibility. COPD is more common among relatives of COPD patients who smoke than unrelated smokers. The genetic differences that make some peoples’ lungs susceptible to the effects of tobacco smoke are mostly unknown. Alpha 1-antitrypsin deficiency is a genetic condition that is responsible for about 2% of cases of COPD. In this condition, the body does not make enough of a protein, alpha 1-antitrypsin. Alpha 1-antitrypsin protects the lungs from damage caused by protease enzymes, such as elastase and trypsin, that can be released as a result of an inflammatory response to tobacco smoke.
Other risk factors
A tendency to sudden airway constriction in response to inhaled irritants, bronchial hyperresponsiveness, is a characteristic of asthma. Many people with COPD also have this tendency. In COPD, the presence of bronchial hyperresponsiveness predicts a worse course of the disease. It is not known if bronchial hyperresponsiveness is a cause or a consequence of COPD. Other risk factors such as repeated lung infection and possibly a diet high in cured meats may be related to the development of COPD.
COPD as an autoimmune disease
Main article: Autoimmunity
There is mounting evidence that there may be an autoimmune component to COPD. Many individuals with COPD who have stopped smoking have active inflammation in the lungs. The disease may continue to get worse for many years after stopping smoking due to this ongoing inflammation. This sustained inflammation is thought to be mediated by autoantibodies and autoreactive T cells.
Disease process
Enlarged view of lung tissue showing the difference between healthy lung and COPD.
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:
Oxidative stress produced by the high concentrations of free radicals in tobacco smoke.
Cytokine release due to inflammation as the body responds to irritant particles such as tobacco smoke in the airway.
Tobacco smoke and free radicals impair the activity of antiprotease enzymes such as alpha 1-antitrypsin, allowing protease enzymes to damage the lung.
Pathology
Chronic bronchitis
Main article: chronic bronchitis
Lung damage and inflammation in the large airways results in chronic bronchitis. 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. In the airways of the lung, the hallmark of chronic bronchitris is an increased number (hyperplasia) and increased size (hypertrophy) of the goblet cells and mucous glands of the airway. As a result, there is more mucus than usual in the airways, contributing to narrowing of the airways and causing a cough with sputum. Microscopically there is infiltration of the airway walls with inflammatory cells. Inflammation is followed by scarring and remodeling that thickens the walls and also results in narrowing of the airways. As chronic bronchitis progresses, there is squamous metaplasia (an abnormal change in the tissue lining the inside of the airway) and fibrosis (further thickening and scarring of the airway wall). The consequence of these changes is a limitation of airflow.
Patients with advanced COPD that have primarily chronic bronchitis rather than emphysema were commonly referred to as “blue bloaters” because of the bluish color of the skin and lips (cyanosis) seen in them. The hypoxia and fluid retention leads to them being called “Blue Bloaters.”
Emphysema
Gross pathology of a lung showing centrilobular-type emphysema characteristic of smoking. This close-up of the fixed, cut lung surface shows multiple cavities lined by heavy black carbon deposits.
Main article: emphysema
Lung damage and inflammation of the air sacs (alveoli) results in emphysema. Emphysema is defined as enlargement of the air spaces distal to the terminal bronchioles, with destruction of their walls. The destruction of air space walls reduces the surface area available for the exchange of oxygen and carbon dioxide during breathing. It also reduces the elasticity of the lung itself, which results in a loss of support for the airways that are embedded in the lung. These airways are more likely to collapse causing further limitation to airflow. The effort made by patients suffering from emphysema during exhalation, causes a pink color in their faces, hence the term commonly used to refer to them, “pink puffers”.
Pathophysiology
Narrowing of the airways reduces the rate at which air can flow to and from the air sacs (alveoli) and limits the 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 has to be faster. A little of the air of the previous breath remains within the lungs when the next breath is started. When this happens, there is an increase in the volume of air in the lungs, a process called dynamic hyperinflation.
Dynamic hyperinflation is closely linked to shortness of breath (dyspnea) 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 gasses 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 dyspnea 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.
Acute exacerbations of COPD
Main article: Acute exacerbation of chronic obstructive pulmonary disease
An acute exacerbation of COPD is a sudden worsening of COPD symptoms (shortness of breath, quantity and color of phlegm) that typically lasts for several days. It may be triggered by an infection with bacteria or viruses or by environmental pollutants. Typically, infections cause 75% or more of the exacerbations; bacteria can roughly be found in 25% of cases, viruses in another 25%, and both viruses and bacteria in another 25%. Pulmonary Embolism can also cause exacerbations of COPD. Airway inflammation is increased during the exacerbation resulting in increased hyperinflation, reduced expiratory air flow and worsening of gas transfer.
Diagnosis
The diagnosis of COPD should be considered in anyone who has dyspnea, chronic cough or sputum production, and/or a history of exposure to risk factors for the disease such as regular tobacco smoking. No single symptom or sign can adequately confirm or exclude the diagnosis of COPD although COPD is uncommon under the age of 40 years.
Spirometry
The diagnosis of COPD is confirmed by spirometry, a test that measures breathing. 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 large 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 (i.e. the FEV1/FVC ratio is >70%). In COPD, this ratio is less than normal, (i.e. FEV1/FVC ratio is <70%) even after a bronchodilator medication has been given.
Spirometry can help to determine the severity of COPD. The FEV1 (measured post-bronchodilator) is expressed as a percent of a predicted “normal” value based on a person’s age, gender, height and weight:
The severity of COPD also depends on the severity of dyspnea and exercise limitation. These and other factors can be combined with spirometry results to obtain a COPD severity score that takes multiple dimensions of the disease into account.
Other tests
An x-ray of the chest may show an over-expanded lung (hyperinflation) and can be useful to help exclude other lung diseases. 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.
A blood sample taken from an artery can be tested for blood gas levels which may show low oxygen levels (hypoxemia) and/or high carbon dioxide levels (respiratory acidosis). A blood sample taken from a vein may show a high blood count (reactive polythycaemia), a reaction to long-term hypoxemia.
Management
There is currently no cure for COPD; however, COPD is both a preventable and treatable disease. Clinical practice guidelines for the management of COPD are available from the Global Initiative for Chronic Obstructive Lung Disease (GOLD), a collaboration that includes the World Health Organization and the U.S. National Heart, Lung, and Blood Institute. The major current directions of COPD management are to assess and monitor the disease, reduce the risk factors, manage stable COPD, prevent and treat acute exacerbations and manage comorbidity.
Risk factor reduction
Smoking cessation
Main article: Smoking cessation
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 anti-smoking organizations can reduce smoking rates by encouraging smoking cessation and discouraging people from starting smoking. These policies are important strategies in the prevention of COPD.
Occupational health
Measures can be taken to reduce the likelihood that workers in at-risk industries such as coal mining will develop COPD. Some examples of these measures are: education of workers and management about the risks, promoting smoking cessation, surveillance of workers for early signs of COPD, the use of personal dust monitors, the 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 pollution
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.
Management of stable COPD
Bronchodilators
Bronchodilators are medicines that relax smooth muscle around the airways, increasing the calibre of the airways and improving air flow. They can reduce the symptoms of shortness of breath, wheeze and exercise limitation, resulting in an improved quality of life for people with COPD. They do not slow down the rate of progression of the underlying disease. Bronchodilators are usually administered with an inhaler or via a nebulizer.
There are two major types of bronchodilator, β2 agonists and anticholinergics. Anticholinergics appear to be superior to β2 agonists in COPD. Anticholinergeics reduce respiratory deaths while β2 agonists have no effect on respiratory deaths. Each type may be either long-acting (with an effect lasting 12 hours or more) or short-acting (with a rapid onset of effect that does not last as long).
Supplemental oxygen can be given to people with COPD who have low oxygen levels in the body. Oxygen is provided from an oxygen cylinder or an oxygen concentrator and delivered to a person through tubing via a nasal cannula or oxygen mask. Supplemental oxygen does not greatly improve shortness of breath but can allow people with COPD and low oxygen levels to do more exercise and household activity. Long-term oxygen therapy for at least 16 hours a day can improve the quality of life and survival for people with COPD and arterial hypoxemia or with complications of hypoxemia such as pulmonary hypertension, cor pulmonale, or secondary erythrocytosis. High concentrations of supplemental oxygen can lead to the accumulation of carbon dioxide and respiratory acidosis for some people with severe COPD; lower oxygen flow rates are generally safer for these individuals.
Pulmonary rehabilitation
Pulmonary rehabilitation is a program of exercise, disease management and counseling coordinated to benefit the individual. Pulmonary rehabilitation has been shown to improve shortness of breath and exercise capacity. It has also been shown to improve the sense of control a patient has over their disease as well as their emotions.
Nutrition
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.
Cold Weather Protection
One of the major winter hazards for individuals with respiratory problems is breathing cold air. Unfortunately, for many people with COPD, breathing cold air causes bronchospasm and increases breathlessness.
Knowing how to manage your symptoms and protect against breathing cold air in the winter can help prevent serious breathing problems, like exacerbations. Exacerbations are particularly common in the winter months causing a significant rise in COPD hospital admissions.
The common cold or other forms of respiratory tract infections may also be potentially serious for the COPD patient. Many respiratory tract infections are contagious and are often spread by simple contact between people. During the winter, the incidence of the common cold and upper respiratory tract infections is much higher than during other times of the year.
For a person with COPD, it is important to make every effort to maintain a healthy lifestyle and enjoy the things you like to do. The cold weather season is no different. To keep active outside during fall and winter, however, people with COPD must be extra cautious in dressing appropriately for cold temperatures.
Appropriate insulated winter clothing is a must! Keeping your head and face warm is extremely important. Even during short exposures your body can lose a lot of heat and energy if it is not properly protected.
Have annual flu and pneumonia vaccinations and take extra precautions to avoid exposure to possible contaminates. One of the simplest things you can do to protect from catching a cold is to wash your hands regularly. Avoiding contact with people who are suffering from a cold also will greatly reduce your risks. Drinking lots of fluids is particularly beneficial during cold weather; a properly hydrated body can better defend against infections and the typical common cold virus.
One way to help improve comfort during cold exposure is to wear a facemask designed to warm the air you breathe. COPD patients can benefit from using a facemask during fall and winter exposures to cold air, as it will help them enjoy advanced protection against cold weather hazards.
Surgery
Surgery is sometimes helpful for COPD in selected cases. A bullectomy is the surgical removal of a bulla, a large air-filled space that can squash the surrounding, more normal lung. Lung volume reduction surgery is similar; parts of the lung that are particularly damaged by emphysema are removed allowing the remaining, relatively good lung to expand and work better. Lung transplantation is sometimes performed for severe COPD, particularly in younger individuals.
Management of acute exacerbations
Acute exacerbations can be partially prevented. Infections are responsible for approximately half of COPD exacerbations, some of which can be prevented by vaccination against pathogens such as influenza and Streptococcus pneumoniae. Regular medication use can prevent some COPD exacerbations; LABAs, long-acting anticholinergics, inhaled corticosteroids and low-dose theophylline have all been shown to reduce the frequency of COPD exacerbations. The symptoms of acute exacerbations are treated using short-acting bronchodilators. A course of corticosteroids, usually in tablet or intravenous rather than inhaled form, can speed up recovery. Antibiotics are often used but will only help if the exacerbation is due to an infection. Antibiotics are indicated when a patient notes sputum changes, has an elevated white count, or is febrile. Severe exacerbations can require hospital care where treatments such as oxygen and mechanical ventilation may be required.
Prognosis
COPD usually gradually gets worse over time and can lead to death. The rate at which it gets worse varies between individuals. The factors that predict a poorer prognosis are:
Severe airflow obstruction (low FEV1)
Poor exercise capacity
Shortness of breath
Significantly underweight or overweight
Complications like respiratory failure or cor pulmonale
Continued smoking
Frequent acute exacerbations
History
COPD has probably always existed but has been called by different names in the past. Bonet described a condition of “voluminous lungs” in 1679. In 1769, Giovanni Morgagni 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.”History of pathologic descriptions of COPD” (PDF).
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 recognized 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.
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Quit Smoking Effects
Many of us worry so much about the effects, or withdrawal symptoms if we quit smoking that we never really try. This page covers the quit smoking effects. It’s part of our Tips To Quit Smoking pages, including 20 Reasons To Quit Smoking, Ways To Quit Smoking, and Quit Smoking Aids.
Any time you change something in your body, the body reacts. When you quit drinking coffee and other caffeinated drinks, you get headaches and sometimes sleepiness. When most of us started smoking, we coughed, sneezed, had headaches and almost vomited…but we wanted to smoke enough to tolerate these bodily reactions. A few weeks later, we wondered what all the fuss was about because all those symptoms disappeared and we regularly lit up with our friends. For me, it was basically the same thing when I quit smoking 16 years ago. I was very uncomfortable for about a week, mildly uncomfortable for the next 2-3 weeks and never had the desire for a cigarette after 3 months. I’ve learned, since, that my experience was about normal. To help you understand what happens, here are some recent popular books on quit smoking withdrawal effects.
When you quit smoking, the hardest thing is deciding.
The quit smoking effects, or withdrawal symptoms, may vary somewhat from person to person, but almost all people are through the worst of it in a week or two. Here’s what most people can expect the first week: Heightened nervousness and anxiety feelings, possible sleep difficulties, irritability and impatience, frequent and repetitive strong cravings to smoke. A few people experience occasional headaches and or nausea during the first week. After the first week, you should have no physical withdrawal symptoms. What most people can expect the second and third weeks are slightly elevated anxiety and irritability and frequent normal desires to smoke. If you have not gone back to cigarettes, your desire for cigarettes and your irritability and anxiety will drop dramatically between 3 weeks and 3 months. After 3 months, most people are amazed at how easy it was to quit smoking and very excited at what’s happening to their body.
About 1-3 months after quitting, you should begin to experience some very surprising things. Your lips, fingers, toes, ears and other appendages will have sensations and feelings you forgot was normal…a whole new level of sensitivity. At about 3 months, you will notice flavors in your food and drinks that you didn’t know were always there. This is when many people replace tobacco addiction with food addiction and begin gaining weight. A great many people keep smoking because of the fear of weight gain. You don’t have to gain weight. I lost 30 pounds during the 3 months after I quit smoking. You can do the same thing by reducing the fat, sugar and salt in your diet about 1 month after you quit smoking. Because you’re more sensitive to taste, you won’t notice the flavor change. Slowly add aerobic exercise at about 3 months to fully capitalize on this opportunity.
From 3 months after you quit smoking, you’ll notice that when you think about cigarettes it won’t be a craving…just an odd thought you easily dismiss. You may or may not notice that the nagging cough is gone. You’ll gradually increase in stamina and energy. If you’re like me, a year after you quit, you won’t be able to remember the last time you wanted a cigarette. You’ll come across a smoker and almost gag yourself because of the smell. Then you’ll realize that’s the way you smelled just a year ago. Be patient with them and pray they find the courage to quit…like you did.
Finally, sometimes we need more help to quit smoking than information, aids and methods provide. Smoking is an addiction. Like any other addiction, sometimes it requires healing the underlying cause before we can end the addiction. Addiction is caused by an emptiness or low self-esteem that causes us to use substances to try and fill the void. The only One who can fill this void in us is God.
Addiction Recovery Support Forum - Help from others in recovery from alcoholism, drugs, sex, gambling, food, codependency and other addictions.
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AFTER YOU STOP SMOKING
In 20 minutes your blood pressure will drop back down to normal.
In 8 hours the carbon monoxide (a toxic gas) levels in your blood stream will drop by half, and oxygen levels will return to normal.
In 48 hours your chance of having a heart attack will have decreased. All nicotine will have left your body. Your sense of taste and smell will return to a normal level.
In 72 hours your bronchial tubes will relax, and your energy levels will increase.
In 2 weeks your circulation will increase, and it will continue to improve for the next 10 weeks.
In three to nine months coughs, wheezing and breathing problems will dissipate as your lung capacity improves by 10%.
In 1 year your risk of having a heart attack will have dropped by half.
In 5 years your risk of having a stroke returns to that of a non-smoker.
In 10 years your risk of lung cancer will have returned to that of a non-smoker. In 15 years your risk of heart attack will have returned to that of a non-smoker.
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