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.

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 laceration is a chest injury in which lung tissue is torn or cut. An injury that is potentially more serious than pulmonary contusion, pulmonary laceration involves disruption of the architecture of the lung, while pulmonary contusion does not. Pulmonary laceration is commonly caused by penetrating trauma but may also result from forces involved in blunt trauma such as shear stress. A cavity filled with blood, air, or both can form. The injury is diagnosed when collections of air or fluid are found on a CT scan of the chest. Surgery may be required to stitch the laceration, to drain blood, or even to remove injured parts of the lung. The injury commonly heals quickly with few problems if it is given proper treatment; however it may be associated with scarring of the lung or other complications.

In 1988, a group led by R.B. Wagner divided pulmonary lacerations into four types based on the manner in which the person was injured and indications found on a CT scan. In type 1 lacerations, which occur in the mid lung area, the air-filled lung bursts as a result of sudden compression of the chest. Also called compression-rupture lacerations, type 1 are the most common type and usually occur in a central location of the lung. They tend to be large, ranging in size from 2–8 cm. The shearing stress in type 2 results when the lower chest is suddenly compressed and the lower lung is suddenly moved across the vertebral bodies. Type 2, also called compression-shear, tends to occur near the spine and have an elongated shape. Type 2 lacerations usually occur in younger people with more flexible chests. Type 3, which are caused by punctures from fractured ribs, occur in the area near the chest wall underlying the broken rib. Also called rib penetration lacerations, type 3 lacerations tend to be small and accompanied by pneumothorax. Commonly, more than one type 3 laceration will occur. Type 4, also called adhesion tears, occur in cases where a pleuropulmonary adhesion had formed prior to the injury, in which the chest wall is suddenly fractured or pushed inwards. They occur in the subpleural area and result from shearing forces at sites of transpleural adhesion.

Signs and symptoms vary depending on what part of the tracheobronchial tree is injured and how severely it is damaged. There are no direct signs of TBI, but certain signs suggest the injury and raise a clinician's suspicion that it has occurred. Many of the signs and symptoms are also present in injuries with similar injury mechanisms such as pneumothorax. Dyspnea and respiratory distress are found in 76–100% of people with TBI, and coughing up blood has been found in up to 25%. However, isolated TBI does not usually cause profuse bleeding; if such bleeding is observed it is likely to be due to another injury such as a ruptured large blood vessel. The patient may exhibit dysphonia or have diminished breath sounds, and rapid breathing is common. Coughing may be present, and stridor, an abnormal, high-pitched breath sound indicating obstruction of the upper airway can also occur.

Damage to the airways can cause subcutaneous emphysema (air trapped in the subcutaneous tissue of the skin) in the abdomen, chest, neck, and head. Subcutaneous emphysema, present in up to 85% of people with TBI, is particularly indicative of the injury when it is only in the neck. Air is trapped in the chest cavity outside the lungs (pneumothorax) in about 70% of TBI. Especially strong evidence that TBI has occurred is failure of a pneumothorax to resolve even when a chest tube is placed to rid the chest cavity of the air; it shows that air is continually leaking into the chest cavity from the site of the tear. Air can also be trapped in the mediastinum, the center of the chest cavity (pneumomediastinum). If air escapes from a penetrating injury to the neck, a definite diagnosis of TBI can be made. Hamman's sign, a sound of crackling that occurs in time with the heartbeat, may also accompany TBI.

A pulmonary hematoma is a collection of blood within the tissue of the lung. It may result when a pulmonary laceration fills with blood. A lung laceration filled with air is called a pneumatocele. In some cases, both pneumatoceles and hematomas exist in the same injured lung. Pulmonary hematomas take longer to heal than simple pneumatoceles and commonly leave the lungs scarred. A pulmonary contusion is another cause of bleeding within the lung tissue, but these result from microhemorrhages, multiple small bleeds, and the bleeding is not a discrete mass but rather occurs within the lung tissue. An indication of more severe damage to the lung than pulmonary contusion, a hematoma also takes longer to clear. Unlike contusions, hematomas do not usually interfere with gas exchange in the lung, but they do increase the risk of infection and abscess formation.

A pneumatocele results when a lung laceration, a cut or tear in the lung tissue, fills with air. A rupture of a small airway creates the air-filled cavity. Pulmonary lacerations that fill with blood are called pulmonary hematomas. In some cases, both pneumatoceles and hematomas exist in the same injured lung. A pneumatocele can become enlarged, for example when the patient is mechanically ventilated or has acute respiratory distress syndrome, in which case it may not go away for months.

A pneumatocele is a cavity in the lung parenchyma filled with air that may result from pulmonary trauma during mechanical ventilation.

Lesions can be transverse, occurring between the rings of the trachea, longitudinal or spiral. They may occur along the membranous part of the trachea, the main bronchi, or both. In 8% of ruptures, lesions are complex, occurring in more than one location, with more than one type of lesion, or on both of the main bronchi and the trachea. Transverse tears are more common than longitudinal or complex ones. The laceration may completely transect the airway or it may go only partway around. Partial tears that do not go all the way around the circumference of the airway do not allow a lacerated airway to become completely detached; tears that encircle the whole airway can allow separation to occur. Lacerations may also be classified as complete or incomplete. In an incomplete lesion, a layer of tissue surrounding the bronchus remains intact and can keep the air in the airway, preventing it from leaking into the areas surrounding the airways. Incomplete lacerations may require closer scrutiny to detect and may not be diagnosed right away.

Bronchial injuries are divided into those that are accompanied by a disruption of the pleura and those that are not; in the former, air can leak from the hole in the airway and a pneumothorax can form. The latter type is associated with more minor signs; pneumothorax is small if it occurs at all, and although function is lost in the part of the lung supplied by the injured bronchus, unaffected parts of the lungs may be able to compensate.

Most TBI that results from blunt trauma occurs within the chest. The most common tracheal injury is a tear near the carina or in the membranous wall of the trachea. In blunt chest trauma, TBI occurs within 2.5 cm of the carina 40–80% of the time. The injury is more common in the right main bronchus than the left, possibly because the former is near vertebrae, which may injure it. Also, the aorta and other tissues in the mid chest that surround the left main bronchus may protect it. Another possibility is that people with left main bronchus injuries are more likely to also have other deadly injuries and therefore die before reaching hospital, making them less likely to be included in studies that determine rates of injuries.

Symptoms can vary greatly, but they include a persistent dry cough.

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.

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.

Failure to have a pulmonary sequestration removed can lead to a number of complications. These include:

- Hemorrhage that can be fatal.

- The creation of a left-right shunt, where blood flows in a shortcut through the feed off the aorta.

- Chronic infection. Diseases such as bronchiectasis, tuberculosis, aspergillosis, bronchial carcinoid and bronchogenic squamous cell carcinoma.

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.

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").

Pulmonary aspiration is the entry of material (such as pharyngeal secretions, food or drink, or stomach contents) from the oropharynx or gastrointestinal tract into the larynx (voice box) and lower respiratory tract (the portions of the respiratory system from the trachea—i.e., windpipe—to the lungs). A person may either inhale the material, or it may be delivered into the tracheobronchial tree during positive pressure ventilation. When pulmonary aspiration occurs during eating and drinking, the aspirated material is often colloquially referred to as "going down the wrong pipe."

Consequences of pulmonary aspiration range from no injury at all, to chemical pneumonitis or pneumonia, to death within minutes from asphyxiation. These consequences depend in part on the volume, chemical composition, particle size, presence or absence of infectious agents, and underlying health status of the person. In healthy people, aspiration of small quantities of material is common and rarely results in disease or injury. People with significant underlying disease or injury, especially hospitalized patients, are at greater risk for developing respiratory complications following pulmonary aspiration because of certain factors such as depressed level of consciousness and impaired airway defenses (gag reflex and/or respiratory tract antimicrobial defense system). As the lumen of the right main bronchus is more vertical and of slightly wider diameter than that of the left, aspirated material is more likely to end up in this bronchus or one of its subsequent .

About 3.6 million cases of pulmonary aspiration or foreign body in the airway occurred in 2013.

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.

Symptoms of pulmonary fibrosis are mainly:

- Shortness of breath, particularly with exertion

- Chronic dry, hacking coughing

- Fatigue and weakness

- Chest discomfort including chest pain

- Loss of appetite and rapid weight loss

Pulmonary fibrosis is suggested by a history of progressive shortness of breath (dyspnea) with exertion. Sometimes fine inspiratory crackles can be heard at the lung bases on auscultation. A chest x-ray may or may not be abnormal, but high-resolution CT will frequently demonstrate abnormalities.

Symptoms of pulmonary embolism are typically sudden in onset and may include one or many of the following: dyspnea (shortness of breath), tachypnea (rapid breathing), chest pain of a "pleuritic" nature (worsened by breathing), cough and hemoptysis (coughing up blood). More severe cases can include signs such as cyanosis (blue discoloration, usually of the lips and fingers), collapse, and circulatory instability because of decreased blood flow through the lungs and into the left side of the heart. About 15% of all cases of sudden death are attributable to PE.

On physical examination, the lungs are usually normal. Occasionally, a pleural friction rub may be audible over the affected area of the lung (mostly in PE with infarct). A pleural effusion is sometimes present that is exudative, detectable by decreased percussion note, audible breath sounds, and vocal resonance. Strain on the right ventricle may be detected as a left parasternal heave, a loud pulmonary component of the second heart sound, and/or raised jugular venous pressure. A low-grade fever may be present, particularly if there is associated pulmonary hemorrhage or infarction.

As smaller pulmonary emboli tend to lodge in more peripheral areas without collateral circulation they are more likely to cause lung infarction and small effusions (both of which are painful), but not hypoxia, dyspnea or hemodynamic instability such as tachycardia. Larger PEs, which tend to lodge centrally, typically cause dyspnea, hypoxia, low blood pressure, fast heart rate and fainting, but are often painless because there is no lung infarction due to collateral circulation. The classic presentation for PE with pleuritic pain, dyspnea and tachycardia is likely caused by a large fragmented embolism causing both large and small PEs. Thus, small PEs are often missed because they cause pleuritic pain alone without any other findings and large PEs often missed because they are painless and mimic other conditions often causing ECG changes and small rises in troponin and BNP levels.

PEs are sometimes described as massive, submassive and nonmassive depending on the clinical signs and symptoms. Although the exact definitions of these are unclear, an accepted definition of massive PE is one in which there is hemodynamic instability such as sustained low blood pressure, slowed heart rate, or pulselessness.

Pulmonary fibrosis (literally "scarring of the lungs") is a respiratory disease in which scars are formed in the lung tissues, leading to serious breathing problems. Scar formation, the accumulation of excess fibrous connective tissue (the process called fibrosis), leads to thickening of the walls, and causes reduced oxygen supply in the blood. As a consequence patients suffer from perpetual shortness of breath.

In some patients the specific cause of the disease can be diagnosed, but in others the probable cause cannot be determined, a condition called idiopathic pulmonary fibrosis. There is no known cure for the scars and damage in the lung due to pulmonary fibrosis.

Pulmonary aspiration is often followed by bacterial pneumonia. Community-acquired aspiration pneumonia is usually caused by anaerobic bacteria, whereas hospital-acquired aspiration pneumonia is more often caused by mixed flora, including both aerobic and anaerobic bacteria.

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.

A chylothorax (or chyle leak) is a type of pleural effusion. It results from lymph formed in the digestive system called chyle accumulating in the pleural cavity due to either disruption or obstruction of the thoracic duct.

In people on a normal diet, this effusion can be identified by its turbid, milky white appearance, since chyle contains high levels of triglycerides. It is important to distinguish chylothorax from pseudochylothorax (pleural effusions high in cholesterol), which has a similar appearance, but is caused by more chronic inflammatory processes, and has a different treatment.

The condition is rare but serious, and appears in all mammals. It results from leakage of lymph fluid from the thoracic duct (or one of its tributaries). This can result from direct laceration (e.g., from surgery) or from nontraumatic causes. The most common nontraumatic cause is malignancy, especially lymphoma. Less common is left-heart failure, infections, and developmental abnormalities such as Down syndrome and Noonan syndrome.