As with other forms of pulmonary edema, the hallmark of SIPE is a cough which may lead to frothy or blood-tinged sputum. Symptoms include:

- Shortness of breath out of proportion to effort being expended.

- Crackles, rattling or ‘junky’ feelings deep in the chest associated with breathing effort – usually progressively worsening with increasing shortness of breath and may be cause for a panic attack

- Cough, usually distressing and productive or not of a little pink, frothy or blood-tinged sputum (hemoptysis)

The wetsuit may feel as though it is hindering breathing ability.

Physiological and symptomatic changes often vary according to the altitude involved.

The Lake Louise Consensus Definition for High-Altitude Pulmonary Edema has set widely used criteria for defining HAPE symptoms:

Symptoms: at least two of:

- Difficulty in breathing (dyspnea) at rest

- Cough

- Weakness or decreased exercise performance

- Chest tightness or congestion

Signs: at least two of:

- Crackles or wheezing (while breathing) in at least one lung field

- Central cyanosis (blue skin color)

- Tachypnea (rapid shallow breathing)

- Tachycardia (rapid heart rate)

The initial cause of HAPE is a shortage of oxygen caused by the lower air pressure at high altitudes.

The mechanisms by which this oxygen shortage causes HAPE are poorly understood, but two processes are believed to be important:

1. Increased pulmonary arterial and capillary pressures (pulmonary hypertension) secondary to hypoxic pulmonary vasoconstriction.

2. An idiopathic non-inflammatory increase in the permeability of the vascular endothelium.

Although higher pulmonary arterial pressures are associated with the development of HAPE, the presence of pulmonary hypertension may not in itself be sufficient to explain the development of edema: severe pulmonary hypertension can exist in the absence of clinical HAPE in subjects at high altitude.

Swimming induced pulmonary edema (SIPE), also known as immersion pulmonary edema, occurs when fluids from the blood leak abnormally from the small vessels of the lung (pulmonary capillaries) into the airspaces (alveoli).

SIPE usually occurs during exertion in conditions of water immersion, such as swimming and diving. With the recent surge in popularity of triathlons and swimming in open water events there has been an increasing incidence of SIPE. It has been reported in scuba divers, apnea (breath hold) free-diving competitors combat swimmers, and triathletes. The causes are incompletely understood at the present time.

High-altitude pulmonary edema (HAPE) ("HAPO" spelled oedema in British English) is a life-threatening form of non-cardiogenic pulmonary edema (fluid accumulation in the lungs) that occurs in otherwise healthy mountaineers at altitudes typically above . However, cases have also been reported at lower altitudes (between in highly vulnerable subjects), though what makes some people susceptible to HAPE is currently unknown. HAPE remains the major cause of death related to high-altitude exposure, with a high mortality rate in the absence of adequate emergency treatment.

The most common symptom of pulmonary edema is difficulty breathing, but may include other symptoms such as coughing up blood (classically seen as pink, frothy sputum), excessive sweating, anxiety, and pale skin. Shortness of breath can manifest as orthopnea (inability to lie down flat due to breathlessness) and/or paroxysmal nocturnal dyspnea (episodes of severe sudden breathlessness at night). These are common presenting symptoms of chronic pulmonary edema due to left ventricular failure. The development of pulmonary edema may be associated with symptoms and signs of "fluid overload"; this is a non-specific term to describe the manifestations of left ventricular failure on the rest of the body and includes peripheral edema (swelling of the legs, in general, of the "pitting" variety, wherein the skin is slow to return to normal when pressed upon), raised jugular venous pressure and hepatomegaly, where the liver is enlarged and may be tender or even pulsatile. Other signs include end-inspiratory crackles (sounds heard at the end of a deep breath) on auscultation and the presence of a third heart sound.

Anaemia that develops gradually usually presents with exertional dyspnea, fatigue, weakness, and tachycardia. It may lead to heart failure. Anaemia caused by low haemoglobin levels is often a cause of dyspnea. Menstruation, particularly if excessive, can contribute to anaemia and to consequential dyspnea in women. Headaches are also a symptom of dyspnea in patients suffering from anaemia. Some patients report a numb sensation in their head, and others have reported blurred vision caused by hypotension behind the eye due to a lack of oxygen and pressure; these patients have also reported severe head pains, many of which lead to permanent brain damage. Symptoms can include loss of concentration, focus, fatigue, language faculty impairment and memory loss.

Other important or common causes of shortness of breath include cardiac tamponade, anaphylaxis, interstitial lung disease, panic attacks, and pulmonary hypertension. Cardiac tamponade presents with dyspnea, tachycardia, elevated jugular venous pressure, and pulsus paradoxus. The gold standard for diagnosis is ultrasound. Anaphylaxis typically begins over a few minutes in a person with a previous history of the same. Other symptoms include urticaria, throat swelling, and gastrointestinal upset. The primary treatment is epinephrine. Interstitial lung disease presents with gradual onset of shortness of breath typically with a history of a predisposing environmental exposure. Shortness of breath is often the only symptom in those with tachydysrhythmias. Panic attacks typically present with hyperventilation, sweating, and numbness. They are however a diagnosis of exclusion. Around 2/3 of women experience shortness of breath as a part of a normal pregnancy. Neurological conditions such as spinal cord injury, phrenic nerve injuries, Guillain–Barré syndrome, amyotrophic lateral sclerosis, multiple sclerosis and muscular dystrophy can all cause an individual to experience shortness of breath. Shortness of breath can also occur as a result of vocal cord dysfunction (VCD).

Presentation may be subtle; people with mild contusion may have no symptoms at all. However, pulmonary contusion is frequently associated with signs (objective indications) and symptoms (subjective states), including those indicative of the lung injury itself and of accompanying injuries. Because gas exchange is impaired, signs of low blood oxygen saturation, such as low concentrations of oxygen in arterial blood gas and cyanosis (bluish color of the skin and mucous membranes) are commonly associated. Dyspnea (painful breathing or difficulty breathing) is commonly seen, and tolerance for exercise may be lowered. Rapid breathing and a rapid heart rate are other signs. With more severe contusions, breath sounds heard through a stethoscope may be decreased, or rales (an abnormal crackling sound in the chest accompanying breathing) may be present. People with severe contusions may have bronchorrhea (the production of watery sputum). Wheezing and coughing are other signs. Coughing up blood or bloody sputum is present in up to half of cases. Cardiac output (the volume of blood pumped by the heart) may be reduced, and hypotension (low blood pressure) is frequently present. The area of the chest wall near the contusion may be tender or painful due to associated chest wall injury.

Signs and symptoms take time to develop, and as many as half of cases are asymptomatic at the initial presentation. The more severe the injury, the more quickly symptoms become apparent. In severe cases, symptoms may occur as quickly as three or four hours after the trauma. Hypoxemia (low oxygen concentration in the arterial blood) typically becomes progressively worse over 24–48 hours after injury. In general, pulmonary contusion tends to worsen slowly over a few days, but it may also cause rapid deterioration or death if untreated.

It might be expected that people with E.I.B. would present with shortness of breath, and/or an elevated respiratory rate and wheezing, consistent with an asthma attack. However, many will present with decreased stamina, or difficulty in recovering from exertion compared to team members, or paroxysmal coughing from an irritable airway. Similarly, examination may reveal wheezing and prolonged expiratory phase, or may be quite normal. Consequently, a potential for under-diagnosis exists. Measurement of airflow, such as peak expiratory flow rates, which can be done inexpensively on the track or sideline, may prove helpful.

Exercise-induced asthma, or E.I.A., occurs when the airways narrow as a result of exercise. The preferred term for this condition is exercise-induced bronchoconstriction (EIB); exercise does not cause asthma, but is frequently an asthma trigger.

Signs that consolidation may have occurred include:

- Expansion of the thorax on inspiration is reduced on the affected side

- Vocal fremitus is increased on the side with consolidation

- Percussion is dull in affected area

- Breath sounds are bronchial

- Possible medium, late, or pan-inspiratory crackles

- Vocal resonance is increased. Here, the patient's voice (or whisper, as in whispered pectoriloquy) can be heard more clearly when there is consolidation, as opposed to in the healthy lung where speech sounds muffled.

- A pleural rub may be present.

- A lower expected Pa02 than calculated in the alveolar gas equation

Pulmonary edema is fluid accumulation in the tissue and air spaces of the lungs. It leads to impaired gas exchange and may cause respiratory failure. It is due to either failure of the left ventricle of the heart to remove blood adequately from the pulmonary circulation (cardiogenic pulmonary edema), or an injury to the lung parenchyma or vasculature of the lung (noncardiogenic pulmonary edema). Treatment is focused on three aspects: firstly improving respiratory function, secondly, treating the underlying cause, and thirdly avoiding further damage to the lung. Pulmonary edema, especially acute, can lead to fatal respiratory distress or cardiac arrest due to hypoxia. It is a cardinal feature of congestive heart failure. The term is from the Greek (oídēma, "swelling"), from οἰδέω (oidéō, "I swell").

The symptoms of pulmonary hypertension include the following:

Less common signs/symptoms include non-productive cough and exercise-induced nausea and vomiting. Coughing up of blood may occur in some patients, particularly those with specific subtypes of pulmonary hypertension such as heritable pulmonary arterial hypertension, Eisenmenger syndrome and chronic thromboembolic pulmonary hypertension. Pulmonary venous hypertension typically presents with shortness of breath while lying flat or sleeping (orthopnea or paroxysmal nocturnal dyspnea), while pulmonary arterial hypertension (PAH) typically does not.

Other typical signs of pulmonary hypertension include an accentuated pulmonary component of the second heart sound, a right ventricular third heart sound, and parasternal heave indicating a hypertrophied right atrium. Signs of systemic congestion resulting from right-sided heart failure include jugular venous distension, ascites, and hepatojugular reflux. Evidence of tricuspid insufficiency and pulmonic regurgitation is also sought and, if present, is consistent with the presence of pulmonary hypertension.

The signs and symptoms of ARDS often begin within two hours of an inciting event, but can occur after 1–3 days. Signs and symptoms may include shortness of breath, fast breathing, and a low oxygen level in the blood due to abnormal ventilation.

The signs and symptoms of PAP include shortness of breath, a cough, low grade fever, and weight loss.

The clinical course of PAP is unpredictable. Spontaneous remission is recognized, and some patients have stable symptoms. Death may occur due to the progression of PAP or of any underlying associated disease. Individuals with PAP are more vulnerable to lung infections such as bacterial pneumonia, mycobacterium avium-intracellulare infection, or a fungal infection.

Pulmonary contusion and laceration are injuries to the lung tissue. Pulmonary laceration, in which lung tissue is torn or cut, differs from pulmonary contusion in that the former involves disruption of the macroscopic architecture of the lung, while the latter does not. When lacerations fill with blood, the result is pulmonary hematoma, a collection of blood within the lung tissue. Contusion involves hemorrhage in the alveoli (tiny air-filled sacs responsible for absorbing oxygen), but a hematoma is a discrete clot of blood not interspersed with lung tissue. A collapsed lung can result when the pleural cavity (the space outside the lung) accumulates blood (hemothorax) or air (pneumothorax) or both (hemopneumothorax). These conditions do not inherently involve damage to the lung tissue itself, but they may be associated with it. Injuries to the chest wall are also distinct from but may be associated with lung injuries. Chest wall injuries include rib fractures and flail chest, in which multiple ribs are broken so that a segment of the ribcage is detached from the rest of the chest wall and moves independently.

A pulmonary consolidation is a region of (normally compressible) lung tissue that has filled with liquid, a condition marked by induration (swelling or hardening of normally soft tissue) of a normally aerated lung. It is considered a radiologic sign. Consolidation occurs through accumulation of inflammatory cellular exudate in the alveoli and adjoining ducts. Simply, it is defined as alveolar space that contains liquid instead of gas. The liquid can be pulmonary edema, inflammatory exudate, pus, inhaled water, or blood (from bronchial tree or hemorrhage from a pulmonary artery). It must be present to diagnose pneumonia: the signs of lobar pneumonia are characteristic and clinically referred to as consolidation.

The symptoms for pulmonary veno-occlusive disease are the following:

Acute respiratory distress syndrome (ARDS) is a medical condition occurring in critically ill patients characterized by widespread inflammation in the lungs. ARDS is not a particular disease; rather, it is a clinical phenotype which may be triggered by various pathologies such as trauma, pneumonia and sepsis.

The hallmark of ARDS is diffuse injury to cells which form the barrier of the microscopic air sacs of the lungs, surfactant dysfunction, activation of the innate immune system response, and dysfunction of the body's regulation of clotting and bleeding. In effect, ARDS impairs the lungs' ability to exchange oxygen and carbon dioxide with the blood across a thin layer of the lungs' microscopic air sacs known as alveoli.

The syndrome is associated with a death rate between 20 and 50%. The risk of death varies based on severity, the person's age, and the presence of other underlying medical conditions.

Although the terminology of "adult respiratory distress syndrome" has at times been used to differentiate ARDS from "infant respiratory distress syndrome" in newborns, the international consensus is that "acute respiratory distress syndrome" is the best term because ARDS can affect people of all ages.

Conditions which commonly involve hemoptysis include bronchitis and pneumonia, lung cancers and tuberculosis. Other possible underlying causes include aspergilloma, bronchiectasis, coccidioidomycosis, pulmonary embolism, pneumonic plague, and cystic fibrosis. Rarer causes include hereditary hemorrhagic telangiectasia (HHT or Rendu-Osler-Weber syndrome), Goodpasture's syndrome, and granulomatosis with polyangiitis. In children, hemoptysis is commonly caused by the presence of a foreign body in the airway. The condition can also result from over-anticoagulation from treatment by drugs such as warfarin.

Blood-laced mucus from the sinus or nose area can sometimes be misidentified as symptomatic of hemoptysis (such secretions can be a sign of nasal or sinus cancer, but also a sinus infection). Extensive non-respiratory injury can also cause one to cough up blood. Cardiac causes like congestive heart failure and mitral stenosis should be ruled out.

The origin of blood can be identified by observing its color. Bright-red, foamy blood comes from the respiratory tract, whereas dark-red, coffee-colored blood comes from the gastrointestinal tract. Sometimes hemoptysis may be rust-colored.

The most common cause of minor hemoptysis is bronchitis.

- Lung cancer, including both non-small cell lung carcinoma and small cell lung carcinoma.

- Sarcoidosis

- Aspergilloma

- Tuberculosis

- Histoplasmosis

- Pneumonia

- Pulmonary edema

- Pulmonary embolism

- Foreign body aspiration and aspiration pneumonia

- Goodpasture's syndrome

- Granulomatosis with polyangiitis

- Eosinophilic granulomatosis with polyangiitis (Churg-Strauss syndrome)

- Bronchitis

- Bronchiectasis

- Pulmonary embolism

- Anticoagulant use

- Trauma

- Lung abscess

- Mitral stenosis

- Tropical eosinophilia

- Bleeding disorders

- Hughes-Stovin Syndrome and other variants of Behçet's disease

- Squamous Cell Carcinoma Of Esophagus

In terms of signs and symptoms the severe form of this condition presents as acute pulmonary heart disease this may lead to death.Clinical fat embolism syndrome presents with tachypnea, elevated temperature, anuria, drowsiness, and occasionally mild neurological symptoms.A petechial rash appears on the upper anterior portion of the body, including the chest, neck, upper arm, oral mucosa and conjunctivae; it appears late and often disappears within hours.

Central nervous system signs in an affected individual include acute confusion, stupor, coma, rigidity (neurology), or convulsions; cerebral edema contributes to the neurologic deterioration.

Embolized fat travels through the venous system to the lungs and can occlude pulmonary capillaries, fat emboli may cause cor pulmonale if adequate compensatory pulmonary vasodilation does not occur.Circulating free fatty acids are directly toxic to pneumocytes and capillary endothelium in the lung, causing interstitial hemorrhage, edema and chemical pneumonitis.Complications from a fat embolism can be serious such as:

1. "Pulmonary fat embolism": Obstruction causes sudden death.

2. "Systemic fat embolism": These may get lodged in capillaries of organs like the brain, kidneys, or skin, causing minute hemorrhage and microinfarcts.

Hemoptysis is the coughing up of blood or blood-stained mucus from the bronchi, larynx, trachea, or lungs. This can occur with lung cancer, infections such as tuberculosis, bronchitis, or pneumonia, and certain cardiovascular conditions. Hemoptysis is considered massive at . In such cases, there are always severe injuries. The primary danger comes from choking, rather than blood loss.

Cardiac asthma is a medical diagnosis of wheezing, coughing or shortness of breath due to congestive heart failure. It is known as cardiac asthma because the symptoms mimic ordinary asthma (bronchial asthma). One study found that patients with cardiac asthma represented one third of congestive heart failure in elderly patients.

Depending on severity, it may be classified as a medical emergency, as it can be a symptom of acute heart failure leading to the buildup of fluid in the lungs (pulmonary edema) as well as within and around the airways.

The distinction between bronchial asthma and cardiac asthma is especially important because some treatments for bronchial asthma, including inhalers, may worsen cardiac asthma or cause severe heart arrhythmias.

Bronchial asthma, in contrast, is caused by the inflammation and narrowing of pulmonary airways, causing the characteristic breathing difficulties. Bronchial asthma has nothing to do with fluid in the lungs or heart disease, or even the heart failure associated with cardiac asthma.

Pulmonary veno-occlusive disease (PVOD) is a rare form of pulmonary hypertension caused by progressive blockage of the small veins in the lungs. The blockage leads to high blood pressures in the arteries of the lungs, which, in turn, leads to heart failure. The disease is progressive and fatal, with median survival of about 2 years from the time of diagnosis to death. The definitive therapy is lung transplantation.