Barotrauma can affect the external, middle, or inner ear. Middle ear barotrauma (MEBT) is the most common being experienced by between 10% and 30% of divers and is due to insufficient equilibration of the middle ear. External ear barotrauma may occur on ascent if high pressure air is trapped in the external auditory canal either by tight fitting diving equipment or ear wax. Inner ear barotrauma (IEBT), though much less common than MEBT, shares a similar mechanism. Mechanical trauma to the inner ear can lead to varying degrees of conductive and sensorineural hearing loss as well as vertigo. It is also common for conditions affecting the inner ear to result in auditory hypersensitivity.

The sinuses similar to other air-filled cavities are susceptible to barotrauma if their openings become obstructed. This can result in pain as well as epistaxis (nosebleed).

Arterial gas embolism (AGE) is a complication of lung barotrauma of ascent. It occurs when breathing gas is introduced to the circulation on the arterial side via lung over-pressure trauma. AGE can present in similar ways to arterial blockages seen in other medical situations. Affected people may suffer strokes, with paralysis or numbness down one side; they may suffer heart attacks; they may suffer pulmonary embolism with shortness of breath and chest pain. It is often impossible to distinguish AGE from DCS, but luckily it is rarely necessary for physicians to be able to distinguish between the two, as treatment is the same. Sometimes AGE and DCS are lumped into a single entity, Decompression Illness (DCI).

Decompression sickness, also called caisson workers' disease and the bends, is the most well-known complication of scuba diving. It occurs as divers ascend, and often from ascending too fast or without doing decompression stops. Bubbles are large enough and numerous enough to cause physical injury. It is quite possible that all divers have microbubbles in their blood to some extent, but that most of the time these bubbles are so few and so small that they cause no harm. When DCS occurs, bubbles disrupt tissues in the joints, brain, spinal cord, lungs, and other organs. Symptoms vary enormously. DCS may be as subtle as unusual tiredness after a dive, or an aching elbow, or a mottled skin rash. Or, it may present dramatically, with unconsciousness, seizures, paralysis, shortness of breath, or death. Paraplegia is not uncommon.

Symptoms of arterial gas embolism include:

- Loss of consciousness

- Cessation of breathing

- Vertigo

- Convulsions

- Tremors

- Loss of coordination

- Loss of control of bodily functions

- Numbness

- Paralysis

- Extreme fatigue

- Weakness in the extremities

- Areas of abnormal sensation

- Visual abnormalities

- Hearing abnormalities

- Personality changes

- Cognitive impairment

- Nausea or vomiting

- Bloody sputum

- Symptoms of other consequences of lung overexpansion such as pneumothorax, subcutaneous or mediastinal emphysema may also be present.

Small amounts of air often get into the blood circulation accidentally during surgery and other medical procedures (for example, a bubble entering an intravenous fluid line), but most of these air emboli enter the veins and are stopped at the lungs, and thus a venous air embolism that shows any symptoms is very rare.

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.

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.

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.

Below is a summary comparison of the signs and symptoms of DCI arising from its two components: "Decompression Sickness" and "Arterial Gas Embolism". Many signs and symptoms are common to both maladies, and it may be difficult to diagnose the actual problem. The dive history can be useful to distinguish which is more probable, but it is possible for both components to manifest at the same time following some dive profiles.

A more detailed account of the signs and symptoms of Decompression Sickness can be found here.

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.

Ventilator-associated lung injury (VALI) is an acute lung injury that develops during mechanical ventilation and is termed ventilator-induced lung injury (VILI) if it can be proven that the mechanical ventilation caused the acute lung injury. In contrast, ventilator-associated lung injury (VALI) exists if the cause cannot be proven. VALI is the appropriate term in most situations because it is virtually impossible to prove what actually caused the lung injury in the hospital.

Subcutaneous emphysema is a common result of certain types of surgery; for example it is not unusual in chest surgery. It may also occur from surgery around the esophagus, and is particularly likely in prolonged surgery. Other potential causes are positive pressure ventilation for any reason and by any technique, in which its occurrence is frequently unexpected. It may also occur as a result of oral surgery, laparoscopy, and cricothyrotomy. In a pneumonectomy, in which an entire lung is removed, the remaining bronchial stump may leak air, a rare but very serious condition that leads to progressive subcutaneous emphysema. Air can leak out of the pleural space through an incision made for a thoracotomy to cause subcutaneous emphysema. On infrequent occasions, the condition can result from dental surgery, usually due to use of high-speed tools that are air driven. These cases result in usually painless swelling of the face and neck, with an immediate onset, the crepitus (crunching sound) typical of subcutaneous emphysema, and often with subcutaneous air visible on X-ray.

One of the main causes of subcutaneous emphysema, along with pneumothorax, is an improperly functioning chest tube. Thus subcutaneous emphysema is often a sign that something is wrong with a chest tube; it may be clogged, clamped, or out of place. The tube may need to be replaced, or, when large amounts of air are leaking, a new tube may be added.

Since mechanical ventilation can worsen a pneumothorax, it can force air into the tissues; when subcutaneous emphysema occurs in a ventilated patient, it is an indication that the ventilation may have caused a pneumothorax. It is not unusual for subcutaneous emphysema to result from positive pressure ventilation. Another possible cause is a ruptured trachea. The trachea may be injured by tracheostomy or tracheal intubation; in cases of tracheal injury, large amounts of air can enter the subcutaneous space. An endotracheal tube can puncture the trachea or bronchi and cause subcutaneous emphysema.

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.

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.

Symptoms and signs of early hypercapnia include flushed skin, full pulse, tachypnea, dyspnea, extrasystoles, muscle twitches, hand flaps, reduced neural activity, and possibly a raised blood pressure. According to other sources, symptoms of mild hypercapnia might include headache, confusion and lethargy. Hypercapnia can induce increased cardiac output, an elevation in arterial blood pressure, and a propensity toward arrhythmias. Hypercapnia may increase pulmonary capillary resistance. In severe hypercapnia (generally PaCO greater than 10 kPa or 75 mmHg), symptomatology progresses to disorientation, panic, hyperventilation, convulsions, unconsciousness, and eventually death.

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.

Tracheobronchial injury (TBI) is damage to the tracheobronchial tree (the airway structure involving the trachea and bronchi). It can result from blunt or penetrating trauma to the neck or chest, inhalation of harmful fumes or smoke, or aspiration of liquids or objects.

Though rare, TBI is a serious condition; it may cause obstruction of the airway with resulting life-threatening respiratory insufficiency. Other injuries accompany TBI in about half of cases. Of those people with TBI who die, most do so before receiving emergency care, either from airway obstruction, exsanguination, or from injuries to other vital organs. Of those who do reach a hospital, the mortality rate may be as high as 30%.

TBI is frequently difficult to diagnose and treat. Early diagnosis is important to prevent complications, which include stenosis (narrowing) of the airway, respiratory tract infection, and damage to the lung tissue. Diagnosis involves procedures such as bronchoscopy, radiography, and x-ray computed tomography to visualize the tracheobronchial tree. Signs and symptoms vary based on the location and severity of the injury; they commonly include dyspnea (difficulty breathing), dysphonia (a condition where the voice can be hoarse, weak, or excessively breathy), coughing, and abnormal breath sounds. In the emergency setting, tracheal intubation can be used to ensure that the airway remains open. In severe cases, surgery may be necessary to repair a TBI.

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.

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.

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.

Hypercapnia is generally caused by hypoventilation, lung disease, or diminished consciousness. It may also be caused by exposure to environments containing abnormally high concentrations of carbon dioxide, such as from volcanic or geothermal activity, or by rebreathing exhaled carbon dioxide. It can also be an initial effect of administering supplemental oxygen on a patient with sleep apnea. In this situation the hypercapnia can also be accompanied by respiratory acidosis.

Decompression Illness (DCI) describes a range of symptoms arising from decompression of the body.

DCI can be caused by two different mechanisms, which result in overlapping sets of symptoms. The two mechanisms are:

- Decompression sickness (DCS), which results from metabolically inert gas dissolved in body tissue under pressure precipitating out of solution and forming bubbles during decompression. It typically afflicts underwater divers on poorly managed ascent from depth or aviators flying in inadequately pressurised aircraft.

- Arterial gas embolism (AGE), which is gas bubbles in the bloodstream. In the context of DCI these may form either as a result of bubble nucleation and growth by dissolved gas into the blood on depressurisation, which is a subset of DCS above, or by gas entering the blood mechanically as a result of pulmonary barotrauma. Pulmonary barotrauma is a rupturing of lung tissue by expansion of breathing gas held in the lungs during depressurisation. This may typically be caused by an underwater diver ascending while holding the breath after breathing at ambient pressure, ambient pressure escape from a submerged submarine without adequate exhalation during the ascent, or the explosive decompression of an aircraft cabin or other pressurised environment.

In any situation which could cause decompression sickness, there is also potentially a risk of arterial gas embolism, and as many of the symptoms are common to both conditions, it may be difficult to distinguish between the two in the field, and first aid treatment is the same for both mechanisms.

VALI does not need to be distinguished from progressive ALI/ARDS because management is the same in both. Additionally, definitive diagnosis of VALI may not be possible because of lack of sign or symptoms.

The term dysbarism encompasses decompression sickness, arterial gas embolism, and barotrauma, whereas decompression sickness and arterial gas embolism are commonly classified together as decompression illness when a precise diagnosis cannot be made. DCS and arterial gas embolism are treated very similarly because they are both the result of gas bubbles in the body. The U.S. Navy prescribes identical treatment for Type II DCS and arterial gas embolism. Their spectra of symptoms also overlap, although those from arterial gas embolism are generally more severe because they often arise from an infarction (blockage of blood supply and tissue death).