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.

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.

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.

Complications are not common but include infection, pulmonary abscess, and bronchopleural fistula (a fistula between the pleural space and the bronchial tree). A bronchopleural fistula results when there is a communication between the laceration, a bronchiole, and the pleura; it can cause air to leak into the pleural space despite the placement of a chest tube. The laceration can also enlarge, as may occur when the injury creates a valve that allows air to enter the laceration, progressively expanding it. One complication, air embolism, in which air enters the bloodstream, is potentially fatal, especially when it occurs on the left side of the heart. Air can enter the circulatory system through a damaged vein in the injured chest and can travel to any organ; it is especially deadly in the heart or brain. Positive pressure ventilation can cause pulmonary embolism by forcing air out of injured lungs and into blood vessels.

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

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.

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 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.

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.

Two of the symptoms of flail chest are chest pain and shortness of breath.

The characteristic paradoxical motion of the flail segment occurs due to pressure changes associated with respiration that the rib cage normally resists:

- During normal inspiration, the diaphragm contracts and intercostal muscles pull the rib cage out. Pressure in the thorax decreases below atmospheric pressure, and air rushes in through the trachea. The flail segment will be pulled in with the decrease in pressure while the rest of the rib cage expands.

- During normal expiration, the diaphragm and intercostal muscles relax increasing internal pressure, allowing the abdominal organs to push air upwards and out of the thorax. However, a flail segment will also be pushed out while the rest of the rib cage contracts.

The constant motion of the ribs in the flail segment at the site of the fracture is extremely painful, and, untreated, the sharp broken edges of the ribs are likely to eventually puncture the pleural sac and lung, possibly causing a pneumothorax. The concern about "mediastinal flutter" (the shift of the mediastinum with paradoxical diaphragm movement) does not appear to be merited. Pulmonary contusions are commonly associated with flail chest and that can lead to respiratory failure. This is due to the paradoxical motions of the chest wall from the fragments interrupting normal breathing and chest movement. Typical paradoxical motion is associated with stiff lungs, which requires extra work for normal breathing, and increased lung resistance, which makes air flow difficult. The respiratory failure from the flail chest requires mechanical ventilation and a longer stay in an intensive care unit. It is the damage to the lungs from the flail segment that is life-threatening.

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.

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

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.

Flail chest is a life-threatening medical condition that occurs when a segment of the rib cage breaks due to trauma and becomes detached from the rest of the chest wall. Two of the symptoms of flail chest are chest pain and shortness of breath.

It occurs when multiple adjacent ribs are broken in multiple places, separating a segment, so a part of the chest wall moves independently. The number of ribs that must be broken varies by differing definitions: some sources say at least two adjacent ribs are broken in at least two places, some require three or more ribs in two or more places. The flail segment moves in the opposite direction to the rest of the chest wall: because of the ambient pressure in comparison to the pressure inside the lungs, it goes in while the rest of the chest is moving out, and vice versa. This so-called "paradoxical breathing" is painful and increases the work involved in breathing.

Flail chest is usually accompanied by a pulmonary contusion, a bruise of the lung tissue that can interfere with blood oxygenation. Often, it is the contusion, not the flail segment, that is the main cause of respiratory problems in people with both injuries.

Surgery to fix the fractures appears to result in better outcomes.

Risk factors for pulmonary aspiration include conditions which depress the level of consciousness (such as traumatic brain injury, alcohol intoxication, drug overdose, and general anesthesia). A decreased gag reflex, upper esophageal sphincter and lower esophageal sphincter tone, gastroesophageal reflux, full stomach, as well as obesity, stroke, and pregnancy can all increase the risk of aspiration in the semiconscious. Tracheal intubation or presence of a gastric tube (for example, a feeding tube) may also increase the risk.

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.

In disorders that are intrinsic to the lung parenchyma, the underlying process is usually pulmonary fibrosis (scarring of the lung). As the disease progresses, the normal lung tissue is gradually replaced by scar tissue interspersed with pockets of air. This can lead to parts of the lung having a honeycomb-like appearance.

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 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.

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.

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.

Restrictive lung diseases (or restrictive ventilatory defects) are a category of extrapulmonary, pleural, or parenchymal respiratory diseases that restrict lung expansion, resulting in a decreased lung volume, an increased work of breathing, and inadequate ventilation and/or oxygenation. Pulmonary function test demonstrates a decrease in the forced vital capacity.

Clinically, IPH manifests as a triad of haemoptysis, diffuse parenchymal infiltrates on chest radiographs, and iron deficiency anaemia. It is diagnosed at an average age of 4.5 plus or minus 3.5 years, and it is twice as common in females. The clinical course of IPH is exceedingly variable, and most of the patients continue to have episodes of pulmonary haemorrhage despite therapy. Death may occur suddenly from acute pulmonary haemorrhage or after progressive pulmonary insufficiency resulting in chronic respiratory failure.

Alveolar disease is visible on chest radiography as small, ill-defined nodules of homogeneous density centered on the acini or bronchioles. The nodules coalesce early in the course of disease, such that the nodules may only be seen as soft fluffy edges in the periphery.

When the nodules are centered on the hilar regions, the chest x-ray may develop what is called the "butterfly," or "batwing" appearance. The nodules may also have a segmental or lobar distribution. Air alveolograms and air bronchograms can also be seen.

These findings appear soon after the onset of symptoms and change rapidly thereafter.

A segmental or lobar pattern may be apparent after aspiration pneumonia, atelectasis, lung contusion, localized pulmonary edema, obstructive pneumonia, pneumonia, pulmonary embolism with infarction, or tuberculosis.