Pulmonary Edema vs. Emphysema

Pulmonary edema is an excess collection of watery fluid in the lungs. This fluid makes it difficult for the lungs to function (to exchange oxygen and carbon dioxide with cells in the bloodstream).

Emphysema is a chronic, progressive lung disease that causes shortness of breath due to over-inflation of the alveoli (air sacs in the lung). In emphysema, the lung tissue involved in the exchange of oxygen and carbon dioxide is damaged or destroyed. Emphysema is in a group of diseases called chronic obstructive pulmonary disease or COPD (pulmonary refers to the lungs).

• The main symptom of pulmonary edema is shortness of breath, which can be severe and patients may feel as if they are downing. Other symptoms of pulmonary edema include coughing up frothy sputum, becoming sweaty and cool and clammy, confusion, lethargy, chest pain, headache, vomiting, and poor decision-making.
• Shortness of breath is also the most common symptom of emphysema. Other symptoms of emphysema include cough, wheezing, decreased tolerance for exercise, "pursed-lip breathing" (a person with emphysema may struggle to exhale completely, in an attempt to empty trapped air. They purse their lips, leaving only a small opening. Then, when they exhale, the lips block the flow of air, increasing pressure in the collapsed airways, and opening them, allowing the trapped air to empty).
• Pulmonary edema is often classified as cardiogenic [due to a heart (cardiac) problem] or non-cardiogenic [due to a non-heart related issue]. Cardiogenic pulmonary edema is the most common type and is sometimes referred to as heart failure or congestive heart failure. Non-cardiogenic pulmonary edema is less common and may be caused by kidney failure, inhaled toxins, high altitude pulmonary edema (HAPE), medication side effects, illicit drug use, adult respiratory distress syndrome (ARDS) or pneumonia.
• The most common cause of emphysema is cigarette smoking. Other risk factors for emphysema include a deficiency of an enzyme called alpha-1-antitrypsin, air pollution, airway reactivity, heredity, male sex, and age.
• Treatment for cardiogenic pulmonary edema includes oxygen, intravenous diuretics, heart medications, and morphine for anxiety. In an emergency situation treatment for pulmonary edema may include positive airway pressure breathing machines (CPAP, BiPAP) or intubation (putting a tube into the airway) and using a ventilator.
• Treatment for acute non-cardiogenic pulmonary edema focuses on decreasing lung inflammation and the short-term use of mechanical ventilation with CPAP, BiPAP, or a ventilator may be used. The underlying cause of pulmonary edema needs to be diagnosed and treated.
• Treatment for emphysema includes quitting smoking, pulmonary rehabilitation (exercise, breathing techniques, education, and therapies), use of medications (including bronchodilators, steroids, and antibiotics), and oxygen. Surgical may be needed in patients with advanced emphysema.
• About half of patients who develop cardiogenic pulmonary edema (heart failure) die within 5 years. The life expectancy varies greatly for patients with non-cardiogenic pulmonary edema depending on the underlying cause.
• Emphysema is the third leading cause of death in the U.S. There is no cure for emphysema, but there are treatments which can slow the progression of the disease.

• Pulmonary edema literally means an excess collection of watery fluid in the lungs. (pulmonary = lung + edema = excess fluid). However, the lung is a complex organ, and there are many causes of this excess fluid accumulation. Regardless of the cause, fluid makes it difficult for the lungs to function (to exchange oxygen and carbon dioxide with cells in the bloodstream).
• Air enters the lungs through the mouth and nose, traveling through the trachea (windpipe) into the bronchial tubes. These tubes branch into progressively smaller segments until they reach blind sacs called alveoli. Here, air is separated from red blood cells in the capillary blood vessels by the microscopically thin walls of the alveolus and the equally thin wall of the blood vessels.
• The walls are so thin that oxygen molecules can leave air and transfer onto the hemoglobin molecule in the red blood cell, in exchange for a carbon dioxide molecule. This allows oxygen to be carried to the body to be used for aerobic metabolism and also allows the waste product, carbon dioxide, to be removed from the body.
• If excess fluid enters the alveolus or if fluid builds up in the space between the alveolar wall and the capillary wall, the oxygen and carbon dioxide molecules have a greater distance to travel and may not be able to be transferred between the lung and bloodstream.
• This lack of oxygen in the bloodstream causes the primary symptom of pulmonary edema, which is shortness of breath.

Emphysema is a long-term, progressive disease of the lungs that primarily causes shortness of breath due to over-inflation of the alveoli (air sacs in the lung). In people with emphysema, the lung tissue involved in exchange of gases (oxygen and carbon dioxide) is impaired or destroyed. Emphysema is included in a group of diseases called chronic obstructive pulmonary disease or COPD (pulmonary refers to the lungs). Emphysema is called an obstructive lung disease because airflow on exhalation is slowed or stopped because over-inflated alveoli do not exchange gases when a person breaths due to little or no movement of gases out of the alveoli.

Emphysema changes the anatomy of the lung in several important ways. This is due to in part to the destruction of lung tissue around smaller airways. This tissue normally holds these small airways, called bronchioles, open, allowing air to leave the lungs on exhalation. When this tissue is damaged, these airways collapse, making it difficult for the lungs to empty and the air (gases) becomes trapped in the alveoli.

Normal lung tissue looks like a new sponge. Emphysematous lung looks like an old used sponge, with large holes and a dramatic loss of “springy-ness” or elasticity. When the lung is stretched during inflation (inhalation), the nature of the stretched tissue wants to relax to its resting state. In emphysema, this elastic function is impaired, resulting in air trapping in the lungs. Emphysema destroys this spongy tissue of the lung and also severely affects the small blood vessels (capillaries of the lung) and airways that run throughout the lung. Thus, not only is airflow affected but so is blood flow. This has dramatic impact on the ability for the lung not only to empty its air sacs called alveoli (pleural for alveolus) but also for blood to flow through the lungs to receive oxygen.

COPD as a group of diseases is one of the leading causes of death in the United States. Unlike heart disease and other more common causes of death, the death rate for COPD appears to be rising.

Pulmonary Edema

Shortness of breath is the most common symptom of pulmonary edema and is due to the failure of the lungs to provide adequate oxygen to the body. In most cases the shortness of breath or dyspnea (dys=abnormal +pnea=breathing) has a gradual onset. However, depending on the cause, it may occur acutely. For example, flash pulmonary edema, which has an abrupt onset, is often associated with a heart attack.

The shortness of breath may initially be manifested by difficulty doing activities that once were routine. There may be a gradual decrease in exercise tolerance, where it takes less activity to bring on symptoms. In addition to shortness of breath, some patients with pulmonary edema will also wheeze.

Orthopnea and paroxysmal nocturnal dyspnea are two variants of shortness of breath seen in association with pulmonary edema.

• Orthopnea describes shortness of breath while lying flat. Some patients with orthopnea may use two or three pillows to prop themselves up at night or resort to sleeping in a recliner.
• Symptoms of paroxysmal nocturnal dyspnea are generally described by the patient as wakening in the middle of the night, short of breath, with a need to walk around and perhaps stand by a window.

The lack of oxygen in the body can cause significant distress, leading to a respiratory crisis, gasping for air, and feeling unable to breathe. In effect, if there is enough fluid in the lungs, it can feel like a drowning. The patient may begin coughing up frothy sputum, become markedly sweaty and cool and clammy. The lack of oxygen can also affect other organs. Confusion and lethargy from lack of oxygen delivery to the brain; and angina (chest pain) from the heart, can both be associated with massive pulmonary edema and respiratory failure.

Pulmonary edema is due to left heart failure, in which pressure backs up into the blood vessels of the lungs, but some patients also have associated right heart failure. In right heart failure, the pressure backs up in the veins of the body, and fluid accumulation can occur in the feet, ankles, and legs as well as any other dependent areas like the sacrum, if the patient sits for prolonged periods of time.

Patients with high altitude pulmonary edema may also develop high altitude cerebral edema (inflammation and swelling of the brain). This may be associated with headache, vomiting, and poor decision making.

Emphysema

Shortness of breath is the most common symptom of emphysema. Cough, sometimes caused by the production of mucus, and wheezing may also be symptoms of emphysema. You may notice that your tolerance for exercise decreases over time. Emphysema usually develops slowly. You may not have any acute episodes of shortness of breath. Slow deterioration is the rule, and it may go unnoticed. This is especially the case if you are a smoker or have other medical problems that limit your ability to exercise.

One of the hallmark signs of emphysema is "pursed-lip breathing." The person with emphysema struggles to exhale completely, in an attempt to empty trapped air. They purse their lips, leaving only a small opening. Then, when they exhale, the lips block the flow of air, increasing pressure in the collapsed airways, and opening them, allowing the trapped air to empty.

People with emphysema may develop a "barrel chest," where the distance from the chest to the back, which is normally less than the distance side to side, becomes more pronounced. This is a direct result of air becoming trapped behind obstructed airways.

Pulmonary Edema

Pulmonary edema is often classified as cardiogenic or non-cardiogenic [due to a heart (cardiac) problem or due to a non-heart related issue respectively].

Cardiogenic Pulmonary Edema

Cardiogenic pulmonary edema is the most common type and is sometimes referred to as heart failure or congestive heart failure.
It may be helpful to understand how blood flows in the body to appreciate why fluid would "back up" into the lungs. The function of the right side of the heart is to receive blood from the body and pump it to the lungs where carbon dioxide is removed, and oxygen is deposited. This freshly oxygenated blood then returns to the left side of the heart which pumps it to the tissues in the body, and the cycle starts again.

Pulmonary edema is a common complication of atherosclerotic (coronary artery) disease. As the blood vessels that supply nutrients to the heart tissue progressively narrow, the heart muscle may not receive enough oxygen and nutrients to pump efficiently and adequately. This can limit the heart's ability to pump the blood it receives from the lungs to the rest of the body. If a heart attack occurs, portions of the heart muscle die and is replaced by scar tissue, further limiting the heart's pumping capability leaving it unable to meet its work requirements.

When the heart muscle is not able to pump effectively there is a back-up of blood returning from the lungs to the heart; this backup causes an increase in pressure within the blood vessels of the lung, resulting in excess fluid leaking from the blood vessels into lung tissue.

Examples of other conditions in which heart muscle may not function adequately include (this list is not all inclusive):

• cardiomyopathy (abnormally functioning heart muscle);
• previous viral infection;
• thyroid problems, and
• alcohol or drug abuse.

Two of the most common cardiomyopathies are ischemic (due to poor blood supply to the heart muscle as described above) and hypertensive. In hypertensive cardiomyopathy, poorly treated high blood pressure results in thickening of the heart muscle to enable the heart to pump blood against that increased pressure. After a period of time, the heart may no longer be able to compensate and fails to keep up with the work load; as a result, fluid leaks out of the blood vessels into the lung tissue.

Another cause of pulmonary edema are mitral and aortic heart valve conditions. Normally, heart valves open and close at the appropriate time when the heart pumps, allowing blood to flow in the appropriate direction. In valvular insufficiency or regurgitation, blood leaks in the wrong direction. In stenosis of the heart valves, the valve becomes narrowed and doesn't allow enough blood to be pumped out of the heart chamber, causing pressure behind it. Failure of the mitral and aortic valves located in the left side of the heart can result in pulmonary edema.

Non-cardiogenic Pulmonary Edema

Non-cardiogenic pulmonary edema is less common and occurs because of damage to the lung tissue and subsequent inflammation of lung tissue. This can cause the tissue that lines the structures of the lung to swell and leak fluid into the alveoli and the surrounding lung tissue. Again, this increases the distance necessary for oxygen to travel to reach the bloodstream.

The following are some examples of causes of non-cardiogenic pulmonary edema.

• Kidney failure: In this situation the kidneys do not remove excess fluid and waste products from the body, and the excess fluid accumulates in the lungs.
• Inhaled toxins: Inhaled toxins (for example, ammonia or chlorine gas, and smoke inhalation) can cause direct damage to lung tissue.
• High altitude pulmonary edema (HAPE): HAPE is a condition that occurs in people whoexercise at altitudes above 8,000ft without having first acclimated to the high altitude. It commonly affects recreational hikers and skiers, but it can also be observed in well-conditioned athletes.
• Medication side effects: These may occur as a complication of aspirin overdose or with the use of somechemotherapy drug treatments.
• Illicit drug use: Non-cardiogenic pulmonary edema is seen in patients who abuse illicit drugs, especially cocaine and heroin.
• Adult respiratory distress syndrome (ARDS): ARDS is a major complication observed in trauma victims, in patients withsepsis, andshock. As part of the body's attempt to respond to a crisis, the antiinflammatory response attacks the lungs with white blood cells and other chemicals of the inflammatory response causing fluid to fill the air spaces of the lungs.
• Pneumonia: Bacterial or viral pneumonia infections are quite common; however, occasionally become complicated as a collection of fluid develops in the section of the lung that is infected.

Emphysema

• Cigarette smoking is by far the most dangerous behavior that causes people to develop emphysema, and it is also the most preventable cause. Other risk factors include a deficiency of an enzyme called alpha-1-antitrypsin, air pollution, airway reactivity, heredity, male sex, and age.
• The importance of cigarette smoking as a risk factor for developing emphysema cannot be overemphasized. Cigarette smoke contributes to this disease process in two ways. It destroys lung tissue, which results in the obstruction of air flow, and it causes inflammation and irritation of airways that can add to air flow obstruction.
• Destruction of lung tissue occurs in several ways. First, cigarette smoke directly affects the cells in the airway responsible for clearing mucus and other secretions. Occasional smoking temporarily disrupts the sweeping action of tiny hairs called cilia that line the airways. Continued smoking leads to longer dysfunction of the cilia. Long-term exposure to cigarette smoke causes the cilia to disappear from the cells lining the air passages. Without the constant sweeping motion of the cilia, mucous secretions cannot be cleared from the lower respiratory tract. Furthermore, smoke causes mucous secretion to be increased at the same time that the ability to clear the secretions is decreased. The resulting mucous buildup can provide bacteria and other organisms with a rich source of food and lead to infection.
• The immune cells in the lung, whose job it is to prevent and fight infection, are also affected by cigarette smoke. They cannot fight bacteria as effectively or clear the lungs of the many particles (such as tar) that cigarette smoke contains. In these ways cigarette smoke sets the stage for frequent lung infections. Although these infections may not even be serious enough to require medical care, the inflammation caused by the immune system constantly attacking bacteria or tar leads to the release of destructive enzymes from the immune cells.
• Over time, enzymes released during this persistent inflammation lead to the loss of proteins responsible for keeping the lungs elastic. In addition, the tissue separating the air cells (alveoli) from one another also is destroyed. Over years of chronic exposure to cigarette smoke, the decreased elasticity and destruction of alveoli leads to the slow destruction of lung function.
• Alpha-1-antitrypsin (also known as alpha-1-antiprotease) is a substance that fights a destructive enzyme in the lungs called trypsin (or protease). Trypsin is a digestive enzyme, most often found in the digestive tract, where it is used to help the body digest food. It is also released by immune cells in their attempt to destroy bacteria and other material. People with alpha-1-antitrypsin deficiency cannot fight the destructive effects of trypsin once it is released in the lung. The destruction of tissue by trypsin produces similar effects to those seen with cigarette smoking. The lung tissue is slowly destroyed, thus decreasing the ability of the lungs to perform appropriately. The imbalance that develops between trypsin and antitrypsin results in an “innocent bystander” effect. Foreign objects (e.g. bacteria) are trying to be destroyed but this enzyme destroys normal tissue since the second enzyme (antiprotease) responsible for controlling the first enzyme (protease) is not available or is poorly functioning. This is referred to as the “Dutch” hypothesis of emphysema formation.
• Air pollution acts in a similar manner to cigarette smoke. The pollutants cause inflammation in the airways, leading to lung tissue destruction.
• Close relatives of people with emphysema are more likely to develop the disease themselves. This is probably because the tissue sensitivity or response to smoke and other irritants may be inherited. The role of genetics in the development of emphysema, however, remains unclear.
• Abnormal airway reactivity, such as bronchial asthma, has been shown to be a risk factor for the development of emphysema.
• Men are more likely to develop emphysema than women. The exact reason for this is unknown, but differences between male and female hormones are suspected.
• Older age is a risk factor for emphysema. Lung function normally declines with age. Therefore, it stands to reason that the older the person, the more likely they will have enough lung tissue destruction to produce emphysema.

It is important to emphasize that COPD is often not purely emphysema or bronchitis, but varying combinations of both.

Pulmonary Edema

Persons who have new, unexplained shortness of breath should seek medical care immediately. If the individual appears to be in distress, the emergency medical system should be activated (call 911 if available). First responders, EMTs, and paramedics can provide life-saving initial treatment on the scene and en-route to a hospital.

For high altitude pulmonary edema, the first treatment goal is to descend and bring the affected person to lower altitude if possible.

When a patient is in respiratory distress, the initial treatment will occur at the same time or even before the diagnosis is made. The health care practitioner will assess whether the airway is open and whether breathing is adequate; otherwise there may be a need to breathe for the patient until treatment becomes effective. The blood pressure may need to be supported with medications until the breathing status improves.

In situations in which there is the luxury of time to evaluate the patient, such as in an office or outpatient clinic, the treatment of pulmonary edema may involve minimizing risk factors that may have caused it.

In cardiogenic pulmonary edema, efforts to maximize heart function and decrease the amount of work the heart has to do are attempted to try to decrease the amount of fluid that the heart has to pump. This should decrease the amount of fluid build-up in the lungs and relieve symptoms.
In the acute situation, oxygen is the first drug that may help reduce dyspnea, or shortness of breath.

Intravenous diuretics [furosemide (Lasix), bumetanide (Bumex)] are first-line medications to help the kidneys remove excess fluid from the body. Even in kidney failure, these drugs may help shift fluid out of the lung for a short period of time.

Reducing the work effort of the heart may be helpful in the acute situation. Nitroglycerin (Nitrolingual, Nitrolingual Duo Pack, Nitroquick, Nitrostat) can be used to reduce the workload of the heart by dilating blood vessels and reducing the amount of blood returning to the heart. Enalapril (Vasotec) and captopril (Capoten) are examples of medications that dilate peripheral arteries and decrease the resistance against which the heart muscle must pump.

Morphine may be considered to ease anxiety and help with the feeling of shortness of breath.

If the patient is in respiratory failure, positive airway pressure breathing machines (CPAP, BiPAP) may be used to force air into the lungs. This is a short-term solution (used for up to a few hours) until the medications work.

In patients who become somnolent (sleepy) or who are no longer able to breathe adequately on their own, intubation (putting a tube into the airway) and using a ventilator may be required.

In non-cardiogenic pulmonary edema, the focus will be on decreasing lung inflammation. While the above medications may be considered, the short-term use of mechanical ventilation with CPAP, BiPAP, or a ventilator may be indicated. The underlying cause of pulmonary edema needs to be diagnosed, and this will direct further therapy.

Emphysema

Treatment for emphysema can take many forms. Different approaches to treatment are available. Generally, a doctor will prescribe these treatments in a step-wise approach, depending on the severity of your condition.

• Stop smoking: Although not strictly a treatment, most doctors make this recommendation for people with emphysema (and everyone). Quitting smoking may halt the progression of the disease and should improve the function of the lungs to some extent. Lung function deteriorates with age. In those susceptible to developing COPD, smoking can result in a five-fold deterioration of lung function. Smoking cessation may return lung function from this rapid deterioration to its normal rate after smoking is stopped. A doctor may be able to prescribe medications to help in breaking the addiction and can also recommend behavioral therapies, such as support groups. You and your doctor should work to find an approach that results in the successful end to cigarette smoking and, in the process, the beginning of improved lung function and quality of life.
• Bronchodilating medications: These medications, which cause the air passages to open more fully and allow better air exchange, are usually the first medications that a doctor will prescribe for emphysema. In very mild cases, bronchodilators may be used only as needed, for episodes of shortness of breath.
  • The most common bronchodilator for mild cases of emphysema is albuterol (Proventil or Ventolin). It acts quickly, and 1 dose usually provides relief for 4-6 hours. Albuterol is most commonly available as a metered-dose inhaler or MDI, and this is the form that is used most often for patients with mild emphysema, with intermittent shortness of breath. When used for this purpose, some people refer to their albuterol inhaler as a "rescue" medication. It acts to rescue them from a more serious attack of shortness of breath.
  • If you have some degree of shortness of breath at rest, a doctor may prescribe the albuterol to be given at regularly scheduled intervals, either through the MDI, or by nebulization. Nebulization involves breathing in liquid medication that has been vaporized by a continuous flow of air (in much the same way a whole-room vaporizer causes liquid droplets to enter the air by the flow of air through water). Nebulized albuterol may be prescribed once scheduled doses via inhaler are no longer adequate to alleviate shortness of breath.
  • Ipratropium bromide (Atrovent) is another bronchodilating medication that is used for relatively mild emphysema. Similar to albuterol, it is available in both an inhaler and as a liquid for nebulization. Unlike albuterol, however, ipratropium bromide is usually given in scheduled intervals. Therefore, it is not usually prescribed for "rescue" purposes. Atrovent lasts longer than albuterol, however, and often provides greater relief. Tiotropium (Spiriva) is a long acting form of ipratropium. This once a day medicine has shown to result in a fewer hospitalizations and possible increased survival in some patients with COPD.
  • Methylxanthines (Theophylline) and other bronchodilating medications are available that have varying properties that may make them useful in certain cases. Theophylline (Theo-Dur, Uniphyl) is a medication given orally (tablets). It can have a sustained effect on keeping air passageways open. Theophylline levels must be monitored by blood tests. This medicine is used less frequently today due to its narrow therapeutic window. Too much theophylline can produce an overdose; too little, and there will not be enough relief of shortness of breath. In addition, other drugs can interact with theophylline, altering the blood level without warning. For this reason, doctors now prescribe theophylline after very carefully considering its potential for other drug interactions. If you take theophylline, take the medication as prescribed and check with your doctor before starting any new medication. Some new studies are suggesting that very low dose theophylline may have anti-inflammatory properties as well. Theophylline used to be widely prescribed; currently it is prescribed infrequently and usually only in special circumstances because of its narrow range of effectiveness, necessity of blood level monitoring and its interactions with other drugs.
• Steroid medications: These decrease inflammation in the body. They are used for this effect in the lung and elsewhere and have been shown to be of some benefit in emphysema. However, not all people will respond to steroid therapy. Steroids may either be given orally or inhaled through an MDI or another form of inhaler.
• Antibiotics: These medications are often prescribed for people with emphysema who have increased shortness of breath. Even when the chest x-ray does not show pneumonia or evidence of infection, people treated with antibiotics tend to have shorter episodes of shortness of breath. It is suspected that infection may play a role in an acute bout of emphysema, even before the infection worsens into a pneumonia or acute bronchitis.
  • Data now suggests that when patients with COPD have a sudden worsening of their symptoms of cough and shortness of breath (also termed an exacerbation), brief and immediate use of steroids and antibiotics can reduce hospitalizations.
• Oxygen: If you have shortness of breath and go to a hospital's emergency department, you often are given oxygen. It may even be necessary to give oxygen by placing a tube in your windpipe and allowing a machine to assist your breathing (also termed tracheal intubation). In some cases, it may be necessary for you to receive oxygen at home as well. There are home-based oxygen tanks available and portable units that enable you to be mobile and engage in normal day-to-day activities.
• Surgical options are available to some people with advanced emphysema.
  • Lung Volume Reduction surgery (LVRS): Although it may not make sense that reducing the size of the lung could help the shortness of breath from emphysema, it is important to remember that emphysema causes an abnormal expansion of the chest wall, which decreases the efficiency of breathing. This surgery is only effective if both upper lobes of the lungs are involved. Removal of this involved lung allows for better expansion of the lower portion of lungs. In a select group of emphysema patients this can improve quality of life for a period of years. Newer studies are underway using one way valves placed in the airways to simulate this volume reduction. The effectiveness of this less invasive procedure is undergoing study at this time.
  • Lung transplant: For people with the most advanced disease, transplantation of either one or both lungs can produce a near-cure. Transplantation brings with it another set of risks and benefits. People who undergo transplantation, however, will have to take medication to prevent the rejection of the transplant by the body. Also, not everyone qualifies for transplantation, and those who do are limited by the short supply of available organs.

Pulmonary rehabilitation is probably the most effective therapy for COPD patients with emphysema. Graded physical exercise, proper breathing techniques, education about the disease and available therapies empowers the patient. It improves quality of life and decreases hospitalizations.

Pulmonary Edema

Cardiogenic pulmonary edema affects up to 2% of the U.S. population and accounts for hundreds of thousands of hospital admissions. Research continues on a variety of medications to help treat patients with acute respiratory distress. New medications such as nesiritide (Natrecor) are being introduced and evaluated to help in the treatment of this disease.

Meanwhile, population education remains the mainstay in trying to decrease the risk of heart disease and the subsequent development of pulmonary edema and heart failure.

Emphysema

Emphysema is a chronic lower respiratory disease, the third leading cause of death in the United States. It is a chronic, progressive disease that affects the quality of life at least as much as the length of life.

Similar to many chronic diseases, the prognosis is affected by too many variables to be discussed here. There is no cure, but there are effective methods of treatment, which can slow the progression of the disease and allow for a normal life.

In short, the diagnosis of emphysema is not a death sentence. Rather, it is a medical condition that should prompt you to take an active role in the management of your disease. Quitting smoking is the best first step. Regular visits to your doctor and taking medications as prescribed are also very important. However, the prognosis decreases if the individual decides to continue to smoke.