A circulatory collapse is defined as a general or specific failure of the circulation, either cardiac or peripheral in nature.

Although the mechanisms, causes and clinical syndromes are different the pathogenesis is the same, the circulatory system fails to maintain the supply of oxygen and other nutrients to the tissues and to remove the carbon dioxide and other metabolites from them. The failure may be hypovolemic, distributive.

A common cause of this could be shock or trauma from injury or surgery.

A "general failure" is one that occurs across a wide range of locations in the body, such as systemic shock after the loss of a large amount of blood collapsing all the circulatory systems in the legs. A "specific failure" can be traced to a particular point, such as a clot.

Cardiac circulatory collapse affects the vessels of the heart such as the aorta and is almost always fatal. It is sometimes referred to as "acute" circulatory failure.

Peripheral circulatory collapse involves outlying arteries and veins in the body and can result in gangrene, organ failure or other serious complications. This form is sometimes called "peripheral vascular failure", "shock" or "peripheral vascular shutdown".

A milder or preliminary form of circulatory collapse is circulatory insufficiency.

Collapse is a sudden and often unannounced loss of postural tone (going weak), often but not necessarily accompanied by loss of consciousness.

If the episode was accompanied by a loss of consciousness, the term syncope is used. The main causes are cardiac (e.g. due to irregular heart beat, low blood pressure), seizures or a psychological cause. The main tool in distinguishing the causes is careful history on the events before, during and after the collapse, from the patient as well as from any possible witnesses. Other investigations may be performed to further strengthen the diagnosis, but many of these have a low yield.

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.

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.

May have no signs and symptoms or they may include:

- cough, but not prominent;

- chest pain (not common);

- breathing difficulty (fast and shallow);

- low oxygen saturation;

- pleural effusion (transudate type);

- cyanosis (late sign);

- increased heart rate.

It is a common misconception that atelectasis causes fever. A study of 100 post-op patients followed with serial chest X-rays and temperature measurements showed that the incidence of fever decreased as the incidence of atelectasis increased. A recent review article summarizing the available published evidence on the association between atelectasis and post-op fever concluded that there is no clinical evidence supporting this doctrine.

Flat-chested kitten syndrome (FCKS), is a disorder in cats, wherein kittens develop a compression of the thorax (chest/ribcage) caused by lung collapse. This is a soft-tissue problem and is not caused by vertebral or bony malformation. However lung collapse can be a secondary symptom caused by bony deformity affecting the thorax such as pectus excavatum. In mild cases, the underside of the chest becomes flattened (hence the name of the condition); in extreme cases the entire thorax is flattened, looking as if the kitten has been stepped on. The kitten will appear to go from normal to flat in the space of about 2–3 hours, and will usually then stabilise.

FCKS is most frequently caused by collapsed lungs (and not as formerly believed, by a muscle spasm in the intercostal muscles). There are numerous causes for lung collapse, and therefore numerous causes for FCKS. One possible cause for flat chestedness that develops soon after birth is atelectasis.

Causes of atelectasis include insufficient attempts at respiration by the newborn, bronchial obstruction, or absence of surfactant (a substance secreted by alveoli that coats the lungs and prevents the surfaces from sticking together). Lack of surfactant reduces the surface area available for effective gas exchange causing lung collapse if severe. There can be many reasons for atelectasis in kittens, but probably the commonest cause is prematurity. Newborn atelectasis would not be unusual in a very large litter of kittens (such as 10), where the size of the litter may lead all the kittens to be small and mildly underdeveloped.

Unlike human babies, kittens are born very immature: blind, deaf, the intestinal tract not fully developed etc., so even slight prematurity may tip them over the edge from being viable to non viable. Many FCKS kittens may have fallen just the wrong side of this boundary in their development at the time of birth. Further, if a kitten does not scream or open its lungs well enough at birth, even if it is fully mature and has sufficient surfactant, it may end up with atelectasis. Patches of atelectasis in the lungs mean that part of a lung is not operating properly. If the kitten goes to sleep and its respiratory rate drops, the patches of atelectasis can slowly expand until large areas of the lung collapse and cannot be reinflated. Good advice to any breeder therefore would be to ensure that kittens cry loudly when they are born, to make sure that the airways are clear, but also that the lungs expand as fully as possible. (This was the reason newborn babies were always held upside down immediately after birth (so that any residual fluid drains downwards) and smacked to make them cry strongly.)

Some kittens suffer from congenital 'secondary' atelectasis, which presents shortly after birth. There have been no reports of kittens born flat (primary atelectasis). Hyaline membrane disease is a type of respiratory distress syndrome of the newborn in which there is formation of a hyaline-like membrane lining the terminal respiratory passages, and this may also be a (rarer) cause of FCKS. Pressure from outside the lung from fluid or air can cause atelectasis as well as obstruction of lung air passages by mucus resulting from various infections and lung diseases – which may explain the development of FCKS in older kittens (e.g. 10 days old) who are not strong enough to breathe through even a light mucus, or who may have inhaled milk during suckling.

Tumors and inhaled objects (possible if bedding contains loose fluff) can also cause obstruction or irritation of the airway, leading to lung collapse and secondary atelectasis. In an older cat the intercostal muscles are so well developed, and the ribs rigid enough that the ribcage will not flatten if the lung collapses: in kittens the bones are much more flexible, and the tendons and muscles more flaccid, allowing movement of the thorax into abnormal positions.

Other causes of lung collapse can include diaphragmatic hernia, or diaphragmatic spasm (breeders report the position of the gut and thorax as appearing to be like a 'stalled hiccup'). Diaphragmatic spasm is easily checked by pinching the phrenic nerve in the neck between the fingertips. Kittens with this type of FCKS will improve almost immediately, but may require repeated pinching to prevent the spasm from recurring.

Initially symptoms asymptomatic or some patients do not experience symptoms at all. In a progressive TBM case symptoms include:

- shortness of breath

- a cough

- mucus build up

- wheezing

- difficulty in breathing

- bluish coloration to skin around the nose and mouth

Symptoms may become worse if the patient is stressed, sick, lying down, or forcing a cough.

- Chronic cough

FCKS develops usually in kittens around three days of age, and sometimes affects whole litters, sometimes only individuals or part of a litter. Kittens can go flat any time during early maturation, some flattening as late as 10 days of age or (in very rare cases) later. It is possible that the later-developing cases are due to Respiratory tract infection or pneumonia. Until 2010 FCKS was believed to be caused by a spasm in the intercostal muscles, but new data has led to the conclusion that flattening is caused by failure of the lungs to inflate normally or, when it occurs in older kittens, by lung collapse.

Gross physical symptoms include flattening of the underside of the thorax in moderate cases (a ridge can usually be felt along the sides of the ribcage, running parallel to the spine); complete flattening of the upper body in extreme cases (the kitten looks as if it has been stepped on); moderate to extreme effort and/or gasping during breathing; the gut is drawn upwards during the in-breath. The position of the thorax and activity of the abdomen is not unlike that seen during normal hiccups, but the sudden spasm in hiccups is slowed down or halted in FCKS: where a hiccup releases, returning the body to a normal position, FCKS breathing does not release. There may be involvement with digestive difficulty in FCKS kittens (see Colic, below).

Determining whether a kitten has FCKS or not can be difficult with only text descriptions: a mild case of FCKS causes the thorax to feel similar to the shape of a banana when held curve downward. The ribcage is not fixed in position, and the most noticeable effect in mild cases is the ridge along the side of the ribcage.

The condition causes weight-gain to halt, respiratory distress, inability to feed normally and, in a significant proportion of cases, death. However, since a significant percentage of kittens survive the condition immediate euthanasia is not indicated, and supportive treatments can be employed to increase the likelihood of survival (see Treatment, below).

The condition is often misdiagnosed as "Pectus excavatum", with which it has no direct connection, although FCKS kittens may also have PE. Although the condition is believed to be more prevalent in the Burmese breed it is found in every breed of cat, including non-pedigree domestic cats, and the apparent prevalence in the Burmese is most likely due to better communication between breeders and reporting of the condition, as well as the naturally more barrel-shaped chest of this particular genotype. Since early reporting of the condition identified the Burmese as susceptible the Bengal breed, with a similar physiology, has emerged, and shows a similarly large number of FCKS kittens, however this may be due to specific interest in the condition among those working with the breeds. It is reported in all breeds and in domestic non-pedigree cats, both those kept as pets and those living as 'barn cats'. An article in a Swedish cat club newsletter about FCKS led to a spike in reporting of the condition in Ragdolls in Sweden.

The syndrome is life-threatening in a significant number of cases (possibly around 50-60%) mainly due to a lack of understanding of the underlying cause of the condition, failure to treat colic (leading to slow starvation) and insufficient sources of information in veterinary literature.

There are three types of tracheomalacia:

- Type 1—congenital, sometimes associated with tracheoesophageal fistula or esophageal atresia

- Type 2—extrinsic compression sometimes due to vascular rings

- Type 3—acquired due to chronic infection or prolonged intubation or inflammatory conditions like relapsing polychondritis

Atelectasis is the collapse or closure of a lung resulting in reduced or absent gas exchange. It may affect part or all of a lung. It is usually unilateral. It is a condition where the alveoli are deflated down to little or no volume, as distinct from pulmonary consolidation, in which they are filled with liquid. It is often called a collapsed lung, although that term may also refer to pneumothorax.

It is a very common finding in chest x-rays and other radiological studies, and may be caused by normal exhalation or by various medical conditions. Although frequently described as a collapse of lung tissue, atelectasis is not synonymous with a pneumothorax, which is a more specific condition that features atelectasis. Acute atelectasis may occur as a post-operative complication or as a result of surfactant deficiency. In premature neonates, this leads to infant respiratory distress syndrome.

The term uses combining forms of "atel-" + "", from , "incomplete" + ἔκτασις, "extension".

Tracheomalacia is a condition where the cartilage that keeps the airway (trachea) open is soft such that the trachea partly collapses especially during increased airflow. The usual symptom is stridor when a person breathes out.

The trachea normally opens slightly during breathing in and narrows slightly during breathing out. These processes are exaggerated in tracheomalacia, leading to airway collapse on breathing out.

If the condition extends further to the large airways (bronchi) (if there is also bronchomalacia), it is termed tracheobronchomalacia. The same condition can also affect the larynx, which is called laryngomalacia. The term is from "trachea" and the Greek μαλακία, "softening"

The diagnosis is made by x-ray/MRI appearance and has five juxta-articular classifications and forehead, neck, and shaft classifications indicating early radiological signs.

Early on there is flattening of articular surfaces, thinning of cartilage with osteophyte (spur) formation. In juxta-articular lesions without symptoms, there is dead bone and marrow separated from living bone by a line of dense collagen. Microscopic cysts form, fill with necrotic material and there is massive necrosis with replacement by cancellous bone with collapse of the lesions.

The lesion begins as a random finding on x-ray without symptoms. Symptomatic lesions usually involve joint surfaces, and fracture with attempted healing occurs. This process takes place over months to years and eventually causes disabling arthritis, particularly of the femoral head (hip).

The following staging system is sometimes useful when managing lesions.

- Stage 0 - Intravascular coagulation

- Stage 1 - Dead Bone without repair

- Stage 2 - Dead Bone with repair but without collapse

- Stage 3 - Dead Bone with repair and with collapse

- Stage 4 - Secondary degenerative arthritis

In a study of bone lesions in 281 compressed air workers done by Walder in 1969, 29% of the lesions were in the humeral head (shoulder), 16% in the femoral head (hip), 40% in the lower end of the femur (lower thigh at the knee) and 15% in the upper tibia (knee below the knee cap).

Worsening of the condition from continued decompression in an asymptomatic x-ray finding may occur.

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.

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.

Collapsed veins are a common result of chronic use of intravenous injections. They are particularly common where injecting conditions are less than ideal, such as in the context of drug abuse.

Veins may become temporarily blocked if the internal lining of the vein swells in response to repeated injury or irritation. This may be caused by the needle, the substance injected, or donating plasma. Once the swelling subsides, the circulation will often become re-established.

Permanent vein collapse occurs as a consequence of:

- Long-term injecting

- Repeated injections, especially with blunt needles

- Poor technique

- Injection of substances which irritate the veins; in particular, injection of liquid methadone intended for oral use.

Smaller veins may collapse as a consequence of too much suction being used when pulling back against the plunger of the syringe to check that the needle is in the vein. This will pull the sides of the vein together and, especially if they are inflamed, they may stick together causing the vein to block. Removing the needle too quickly after injecting can have a similar effect.

Collapsed veins may never recover. Many smaller veins are created by the body to circulate the blood, but they are not adequate for injections or IVs.

Tracheobronchomalacia or TBM is a condition characterized by flaccidity of the tracheal support cartilage which leads to tracheal collapse. This condition can also affect the bronchi. There are two forms of this rare condition: primary TB and secondary TB. Primary TB is congenital and starts as early as two years old. It is mainly linked to genetic causes. Secondary TB is acquired and starts in adulthood. It is mainly developed after an accident or chronic inflammation.

On 28 May 2013, it was reported that a cure had been developed via a 3D printed windpipe. This cure has currently saved the lives of at least 3 infants.

Dysbaric osteonecrosis or DON is a form of avascular necrosis where there is death of a portion of the bone that is thought to be caused by nitrogen embolism (blockage of the blood vessels by a bubble of nitrogen coming out of solution) in divers. Although the definitive pathologic process is poorly understood, there are several hypotheses:

- Intra- or extravascular nitrogen in bones, "nitrogen embolism".

- Osmotic gas effects due to intramedullary pressure effects.

- fat embolism

- hemoconcentration and increased coagulability.

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.

Onset of lung collapse is less than 72 hours after menstruation. Typically, it occurs in women aged 30–40 years, but has been diagnosed in young girls as early as 10 years of age and post menopausal women (exclusively in women of menstrual age) most with a history of pelvic endometriosis.

Abdominal compartment syndrome occurs when the abdomen becomes subject to increased pressure. Specific cause of abdominal compartment syndrome is not known, although some causes can be sepsis and severe abdominal trauma. Increasing pressure reduces blood flow to abdominal organs and impairs pulmonary, cardiovascular, renal, and gastro-intestinal (GI) function, causing multiple organ dysfunction syndrome and death.

Embouchure collapse caused by focal dystonia can be diagnosed medically; embouchure collapse caused by embouchure overuse, however, is generally speaking not considered to be a specifically medical issue. A difficulty in diagnosis is that when a brass player describes the symptoms to a doctor or dentist (as is often the case), the medical practitioner does not fully understand what the patient means. This is because brass players learn their embouchure by "feel," and therefore words have a limited ability to describe embouchure problems, especially if the person listening to the description is not a brass player and has a limited knowledge of the embouchure.

Also, in less severe cases, the player may only be able to feel what is wrong while playing. Many players with an embouchure problem will, once they have realized that it is more than a simple case of tired lips, wish to refrain from playing. The fact that around 24 muscles are employed in forming a brass embouchure, and that each will change slightly as a player struggles to play when experiencing embouchure problems, mean that what players describe as being wrong will have not only worsened their condition when they play, but will be different each time they do so.

In the severest cases, the pain caused by embouchure overuse can be felt even when not playing; in some cases, other symptoms will manifest, such as loss of tissue and damaged nerves. This, however, occurs only in the rarest and most extreme circumstances and usually signals the end of the player's career.

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.

The defining symptom of pleurisy is a sudden sharp, stabbing, burning or dull pain in the right or left side of the chest during breathing, especially when one inhales and exhales. It feels worse with deep breathing, coughing, sneezing, or laughing. The pain may stay in one place, or it may spread to the shoulder or back. Sometimes, it becomes a fairly constant dull ache.

Depending on its cause, pleuritic chest pain may be accompanied by other symptoms:

- Dry cough

- Fever and chills

- Rapid, shallow breathing

- Shortness of breath

- Fast heart rate

- Sore throat followed by pain and swelling in the joints

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