Shortness of breath is often the symptom that most bothers people. It is commonly described as: "my breathing requires effort," "I feel out of breath," or "I can't get enough air in". Different terms, however, may be used in different cultures. Typically the shortness of breath is worse on exertion of a prolonged duration and worsens over time. In the advanced stages, or end stage pulmonary disease it occurs during rest and may be always present. It is a source of both anxiety and a poor quality of life in those with COPD. Many people with more advanced COPD breathe through pursed lips and this action can improve shortness of breath in some.

A chronic cough is often the first symptom to develop. When it persists for more than three months each year for at least two years, in combination with sputum production and without another explanation, it is by definition chronic bronchitis. This condition can occur before COPD fully develops. The amount of sputum produced can change over hours to days. In some cases, the cough may not be present or may only occur occasionally and may not be productive. Some people with COPD attribute the symptoms to a "smoker's cough". Sputum may be swallowed or spat 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 a history of "common colds" that last a long time.

Diagnosis of obstructive disease requires several factors depending on the exact disease being diagnosed. However one commonalty between them is an FEV1/FVC ratio less than 0.7, i.e. the inability to exhale 70% of their breath within one second.

Following is an overview of the main obstructive lung diseases. "Chronic obstructive pulmonary disease" is mainly a combination of chronic bronchitis and emphysema, but may be more or less overlapping with all conditions.

Asthma is an obstructive lung disease where the bronchial tubes (airways) are extra sensitive (hyperresponsive). The airways become inflamed and produce excess mucus and the muscles around the airways tighten making the airways narrower. Asthma is usually triggered by breathing in things in the air such as dust or pollen that produce an allergic reaction. It may be triggered by other things such as an upper respiratory tract infection, cold air, exercise or smoke. Asthma is a common condition and affects over 300 million people around the world.

Asthma causes recurring episodes of wheezing, breathlessness, chest tightness, and coughing, particularly at night or in the early morning.

- Exercise-Induced Asthma — is common in asthmatics, especially after participation in outdoor activities in cold weather.

- Occupational Asthma — An estimated 2% to 5% of all asthma episodes may be caused by exposure to a specific sensitizing agent in the workplace.

- Nocturnal Asthma — is a characteristic problem in poorly controlled asthma and is reported by more than two thirds of sub-optimally treated patients.

A peak flow meter can record variations in the severity of asthma over time. Spirometry, a measurement of lung function, can provide an assessment of the severity, reversibility, and variability of airflow limitation, and help confirm the diagnosis of asthma.

The major signs of indium lung are pulmonary alveolar proteinosis and pulmonary fibrosis. Symptoms include dyspnea (shortness of breath), cough, and increased sputum production. Hemoptysis has also been seen in people with indium lung. Other symptoms seen in some but not all cases include digital clubbing, low DLCO (capacity to move oxygen from the alveoli into the blood), and lowered forced expiratory volume. Emphysema has been associated with indium lung, but may not be part of the syndrome.

Respiratory disease is a medical term that encompasses pathological conditions affecting the organs and tissues that make gas exchange possible in higher organisms, and includes conditions of the upper respiratory tract, trachea, bronchi, bronchioles, alveoli, pleura and pleural cavity, and the nerves and muscles of breathing. Respiratory diseases range from mild and self-limiting, such as the common cold, to life-threatening entities like bacterial pneumonia, pulmonary embolism, acute asthma and lung cancer.

The study of respiratory disease is known as pulmonology. A doctor who specializes in respiratory disease is known as a pulmonologist, a chest medicine specialist, a respiratory medicine specialist, a respirologist or a thoracic medicine specialist.

Respiratory diseases can be classified in many different ways, including by the organ or tissue involved, by the type and pattern of associated signs and symptoms, or by the cause of the disease.

Chronic respiratory diseases (CRDs) are diseases of the airways and other structures of the lung. This disease could be characterized by a high inflammatory cells recruitment (neutrophil) and/or destructive cycle of infection, (e.g. mediated by "Pseudomonas aeruginosa"). Some of the most common are asthma, chronic obstructive pulmonary disease, or acute respiratory distress syndrome . CRDs are not curable, however, various forms of treatment that help dilate major air passages and improve shortness of breath can help control symptoms and increase the quality of life for people with the disease.

it usually lasts for three months to two years

Pulmonary interstitial emphysema is a concern in any of the following diagnosis:

- Prematurity

- Respiratory distress syndrome (RDS)

- Meconium aspiration syndrome (MAS)

- Amniotic fluid aspiration

- Sepsis, or other infections

- Mechanical ventilation

Pulmonary interstitial emphysema (PIE) is a collection of air outside of the normal air space of the pulmonary alveoli, found instead inside the connective tissue of the peribronchovascular sheaths, interlobular septa, and visceral pleura. (This supportive tissue is called the pulmonary interstitium.) This collection of air develops as a result of alveolar and terminal bronchiolar rupture. Pulmonary interstitial emphysema is more frequent in premature infants who require mechanical ventilation for severe lung disease. Infants suffering from pulmonary interstitial emphysema are typically recommended for admission to a neonatal intensive care unit.

Signs and symptoms of spontaneous subcutaneous emphysema vary based on the cause, but it is often associated with swelling of the neck and chest pain, and may also involve sore throat, neck pain, difficulty swallowing, wheezing and difficulty breathing. Chest X-rays may show air in the mediastinum, the middle of the chest cavity. A significant case of subcutaneous emphysema is easy to detect by touching the overlying skin; it feels like tissue paper or Rice Krispies. Touching the bubbles causes them to move and sometimes make a crackling noise. The air bubbles, which are painless and feel like small nodules to the touch, may burst when the skin above them is palpated. The tissues surrounding SCE are usually swollen. When large amounts of air leak into the tissues, the face can swell considerably. In cases of subcutaneous emphysema around the neck, there may be a feeling of fullness in the neck, and the sound of the voice may change. If SCE is particularly extreme around the neck and chest, the swelling can interfere with breathing. The air can travel to many parts of the body, including the abdomen and limbs, because there are no separations in the fatty tissue in the skin to prevent the air from moving.

Indium lung is a rare occupational lung disease caused by exposure to respirable indium in the form of indium tin oxide. It is classified as an interstitial lung disease (diffuse parenchymal lung disease).

According to the International Labour Office (ILO), PMF requires the presence of large opacity exceeding 1 cm (by x-ray). By pathology standards, the lesion in histologic section must exceed 2 cm to meet the definition of PMF. In PMF, lesions most commonly occupy the upper lung zone, and are usually bilateral. The development of PMF is usually associated with a restrictive ventilatory defect on pulmonary function testing. PMF can be mistaken for bronchogenic carcinoma and vice versa. PMF lesions tend to grow very slowly, so any rapid changes in size, or development of cavitation, should prompt a search for either alternative cause or secondary disease.

Subcutaneous emphysema is when gas or air is in the layer under the skin. "Subcutaneous" refers to the tissue beneath the skin, and "emphysema" refers to trapped air. It is sometimes abbreviated SCE or SE and also called tissue emphysema, or Sub Q air. Since the air generally comes from the chest cavity, subcutaneous emphysema usually occurs on the chest, neck and face, where it is able to travel from the chest cavity along the fascia. Subcutaneous emphysema has a characteristic crackling feel to the touch, a sensation that has been described as similar to touching Rice Krispies; this sensation of air under the skin is known as "subcutaneous crepitation".

Numerous etiologies of subcutaneous emphysema have been described. Pneumomediastinum was first recognized as a medical entity by Laennec, who reported it as a consequence of trauma in 1819. Later, in 1939, at The Johns Hopkins Hospital, Dr. Louis Hamman described it in postpartum woman; indeed, subcutaneous emphysema is sometimes known as Hamman's syndrome. However, in some medical circles, it can instead be more commonly known as Macklin's Syndrome after L. Macklin, in 1939, and M.T. and C.C. Macklin, in 1944, who cumulatively went on to describe the pathophysiology in more detail.

Subcutaneous emphysema can result from puncture of parts of the respiratory or gastrointestinal systems. Particularly in the chest and neck, air may become trapped as a result of penetrating trauma (e.g., gunshot wounds or stab wounds) or blunt trauma. Infection (e.g., gas gangrene) can cause gas to be trapped in the subcutaneous tissues. Subcutaneous emphysema can be caused by medical procedures and medical conditions that cause the pressure in the alveoli of the lung to be higher than that in the tissues outside of them. Its most common causes are pneumothorax and a chest tube that has become occluded by a blood clot or fibrinous material. It can also occur spontaneously due to rupture of the alveoli with dramatic presentation. When the condition is caused by surgery it is called "surgical emphysema". The term "spontaneous subcutaneous emphysema" is used when the cause is not clear.

Subcutaneous emphysema is not typically dangerous in and of itself, however it can be a symptom of very dangerous underlying conditions, such as pneumothorax. Although the underlying conditions require treatment, subcutaneous emphysema usually does not; small amounts of air are reabsorbed by the body. However, subcutaneous emphysema can be uncomfortable and may interfere with breathing, and is often treated by removing air from the tissues, for example by using large bore needles, skin incisions or subcutaneous catheterization.

The main symptom is usually severe central chest pain. Other symptoms include laboured breathing, voice distortion (as with helium) and subcutaneous emphysema, specifically affecting the face, neck, and chest. Pneumomediastinum can also be characterized by the shortness of breath that is typical of a respiratory system problem. It is often recognized on auscultation by a "crunching" sound timed with the cardiac cycle (Hamman's crunch).

Pnemomediastinum may also present with symptoms mimicking cardiac tamponade as a result of the increased intrapulmonary pressure on venous flow to the heart.

A primary spontaneous pneumothorax (PSP) tends to occur in a young adult without underlying lung problems, and usually causes limited symptoms. Chest pain and sometimes mild breathlessness are the usual predominant presenting features. People who are affected by PSPs are often unaware of potential danger and may wait several days before seeking medical attention. PSPs more commonly occur during changes in atmospheric pressure, explaining to some extent why episodes of pneumothorax may happen in clusters. It is rare for PSPs to cause tension pneumothoraces.

Secondary spontaneous pneumothoraces (SSPs), by definition, occur in individuals with significant underlying lung disease. Symptoms in SSPs tend to be more severe than in PSPs, as the unaffected lungs are generally unable to replace the loss of function in the affected lungs. Hypoxemia (decreased blood-oxygen levels) is usually present and may be observed as cyanosis (blue discoloration of the lips and skin). Hypercapnia (accumulation of carbon dioxide in the blood) is sometimes encountered; this may cause confusion and – if very severe – may result in comas. The sudden onset of breathlessness in someone with chronic obstructive pulmonary disease (COPD), cystic fibrosis, or other serious lung diseases should therefore prompt investigations to identify the possibility of a pneumothorax.

Traumatic pneumothorax most commonly occurs when the chest wall is pierced, such as when a stab wound or gunshot wound allows air to enter the pleural space, or because some other mechanical injury to the lung compromises the integrity of the involved structures. Traumatic pneumothoraces have been found to occur in up to half of all cases of chest trauma, with only rib fractures being more common in this group. The pneumothorax can be occult (not readily apparent) in half of these cases, but may enlarge - particularly if mechanical ventilation is required. They are also encountered in patients already receiving mechanical ventilation for some other reason.

Upon physical examination, breath sounds (heard with a stethoscope) may be diminished on the affected side, partly because air in the pleural space dampens the transmission of sound. Measures of the conduction of vocal vibrations to the surface of the chest may be altered. Percussion of the chest may be perceived as hyperresonant (like a booming drum), and vocal resonance and tactile fremitus can both be noticeably decreased. Importantly, the volume of the pneumothorax can show limited correlation with the intensity of the symptoms experienced by the victim, and physical signs may not be apparent if the pneumothorax is relatively small.

Although multiple definitions exist, a tension pneumothorax is generally considered to be present when a pneumothorax (primary spontaneous, secondary spontaneous, or traumatic) leads to significant impairment of respiration and/or blood circulation. Tension pneumothorax tends to occur in clinical situations such as ventilation, resuscitation, trauma, or in patients with lung disease.

The most common findings in people with tension pneumothorax are chest pain and respiratory distress, often with an increased heart rate (tachycardia) and rapid breathing (tachypnea) in the initial stages. Other findings may include quieter breath sounds on one side of the chest, low oxygen levels and blood pressure, and displacement of the trachea away from the affected side. Rarely, there may be cyanosis (bluish discoloration of the skin due to low oxygen levels), altered level of consciousness, a hyperresonant percussion note on examination of the affected side with reduced expansion and decreased movement, pain in the epigastrium (upper abdomen), displacement of the apex beat (heart impulse), and resonant sound when tapping the sternum. This is a medical emergency and may require immediate treatment without further investigations (see below).

Tension pneumothorax may also occur in someone who is receiving mechanical ventilation, in which case it may be difficult to spot as the person is typically receiving sedation; it is often noted because of a sudden deterioration in condition. Recent studies have shown that the development of tension features may not always be as rapid as previously thought. Deviation of the trachea to one side and the presence of raised jugular venous pressure (distended neck veins) are not reliable as clinical signs.

Patients with subacute HP gradually develop a productive cough, dyspnea, fatigue, anorexia, weight loss, and pleurisy. Symptoms are similar to the acute form of the disease, but are less severe and last longer. On chest radiographs, micronodular or reticular opacities are most prominent in mid-to-lower lung zones. Findings may be present in patients who have experienced repeated acute attacks.

The subacute, or intermittent, form produces more well-formed noncaseating granulomas, bronchiolitis with or without organizing pneumonia, and interstitial fibrosis.

Progressive Massive Fibrosis (PMF), characterized by the development of large conglomerate masses of dense fibrosis (usually in the upper lung zones), can complicate silicosis and coal worker's pneumoconiosis. Conglomerate masses may also occur in other pneumoconioses, such as talcosis, berylliosis (CBD), kaolin pneumoconiosis, and pneumoconiosis from carbon compounds, such as carbon black, graphite, and oil shale. Conglomerate masses can also develop in sarcoidosis, but usually near the hilae and with surrounding paracitricial emphysema.

The disease arises firstly through the deposition of silica or coal dust (or other dust) within the lung, and then through the body's immunological reactions to the dust.

In chronic HP, patients often lack a history of acute episodes. They have an insidious onset of cough, progressive dyspnea, fatigue, and weight loss. This is associated with partial to complete but gradual reversibility. Avoiding any further exposure is recommended. Clubbing is observed in 50% of patients. Tachypnea, respiratory distress, and inspiratory crackles over lower lung fields often are present.

On chest radiographs, progressive fibrotic changes with loss of lung volume particularly affect the upper lobes. Nodular or ground-glass opacities are not present. Features of emphysema are found on significant chest films and CT scans.

Chronic forms reveal additional findings of chronic interstitial inflammation and alveolar destruction (honeycombing) associated with dense fibrosis. Cholesterol clefts or asteroid bodies are present within or outside granulomas.

In addition, many patients have hypoxemia at rest, and all patients desaturate with exercise.

Pneumomediastinum (from Greek "pneuma" – "air", also known as mediastinal emphysema) is (abnormal presence of air or other gas) in the mediastinum. First described in 1819 by René Laennec, the condition can result from physical trauma or other situations that lead to air escaping from the lungs, airways, or bowel into the chest cavity.

Symptoms of alpha-1 antitrypsin deficiency include shortness of breath, wheezing, rhonchi, and rales. The patient's symptoms may resemble recurrent respiratory infections or asthma that does not respond to treatment. Individuals with A1AD may develop emphysema during their thirties or forties even without a history of significant smoking, though smoking greatly increases the risk for emphysema. A1AD causes impaired liver function in some patients and may lead to cirrhosis and liver failure (15%).

In newborns, alpha-1 antitrypsin deficiency has indicators that include early onset jaundice followed by prolonged jaundice. It is a leading indication for liver transplantation in newborns.

Aspergillosis is an infection caused by the fungus "Aspergillus". Aspergillosis describes a large number of diseases involving both infection and growth of fungus as well as allergic responses. Aspergillosis can occur in a variety of organs, both in humans and animals.

The most common sites of infection are the respiratory apparatus (lungs, sinuses) and these infections can be:

- Invasive (e.g. – IPA)

- Non-invasive (e.g. Allergic Pulmonary Aspergillosis - ABPA)

- Chronic pulmonary and aspergilloma (e.g. chronic cavitary, semi-invasive)

- Severe asthma with fungal sensitisation (SAFS)

Chronic pulmonary aspergillosis (CPA) is a long-term aspergillus infection of the lung and "Aspergillus fumigatus" is almost always the species responsible for this illness. Patients fall into several groups as listed below.

- Those with an aspergilloma which is a ball of fungus found in a single lung cavity - which may improve or disappear, or change very little over a few years.

- Aspergillus nodule

- Chronic cavitary pulmonary aspergillosis (CCPA) where cavities are present in the lungs, but not necessarily with a fungal ball (aspergilloma).

- Chronic fibrosing pulmonary aspergillosis this may develop where pulmonary aspergillosis remains untreated and chronic scarring of the lungs occurs. Unfortunately scarring of the lungs does not improve.

Most patients with CPA have or have had an underlying lung disease. The most common diseases include tuberculosis, atypical mycobacterium infection, stage III fibrocystic pulmonary sarcoidosis, ABPA, lung cancer, COPD and emphysema, asthma and silicosis.

Initially, the disease appears as alveolitis, and then progresses to emphysema.

Patients may develop pneumothorax (collapsed lung).

Congenital lobar emphysema (CLE), also known as congenital lobar overinflation and infantile lobar emphysema, is a neonatal condition associated with enlarged air spaces in the lungs of newborn children. It is diagnosed around the time of birth or in the first 6 months of life, occurring more often in boys than girls. CLE affects the upper lung lobes more than the lower lobes, and the left lung more often than the right lung. Although CLE may be caused by abnormal development of airways (bronchi, for example) or compression of airways by nearby tissues, no cause is identified in half of cases.

Classification of silicosis is made according to the disease's severity (including radiographic pattern), onset, and rapidity of progression. These include:

- Chronic simple silicosis: Usually resulting from long-term exposure (10 years or more) to relatively low concentrations of silica dust and usually appearing 10–30 years after first exposure. This is the most common type of silicosis. Patients with this type of silicosis, especially early on, may not have obvious signs or symptoms of disease, but abnormalities may be detected by x-ray. Chronic cough and exertional dyspnea (shortness of breath) are common findings. Radiographically, chronic simple silicosis reveals a profusion of small (<10 mm in diameter) opacities, typically rounded, and predominating in the upper lung zones.

- Accelerated silicosis: Silicosis that develops 5–10 years after first exposure to higher concentrations of silica dust. Symptoms and x-ray findings are similar to chronic simple silicosis, but occur earlier and tend to progress more rapidly. Patients with accelerated silicosis are at greater risk for complicated disease, including progressive massive fibrosis (PMF).

- Complicated silicosis: Silicosis can become "complicated" by the development of severe scarring (progressive massive fibrosis, or also known as conglomerate silicosis), where the small nodules gradually become confluent, reaching a size of 1 cm or greater. PMF is associated with more severe symptoms and respiratory impairment than simple disease. Silicosis can also be complicated by other lung disease, such as tuberculosis, non-tuberculous mycobacterial infection, and fungal infection, certain autoimmune diseases, and lung cancer. Complicated silicosis is more common with accelerated silicosis than with the chronic variety.

- Acute silicosis: Silicosis that develops a few weeks to 5 years after exposure to high concentrations of respirable silica dust. This is also known as silicoproteinosis. Symptoms of acute silicosis include more rapid onset of severe disabling shortness of breath, cough, weakness, and weight loss, often leading to death. The x-ray usually reveals a diffuse alveolar filling with air bronchograms, described as a ground-glass appearance, and similar to pneumonia, pulmonary edema, alveolar hemorrhage, and alveolar cell lung cancer.