A very large range of medical conditions can cause circulatory collapse. These include, but are not limited to:

- Surgery, particularly on patients who have lost blood.

- Blood clots, including the use of some platelet-activating factor drugs in some animals and humans

- Dengue Fever

- Severe dehydration

- Shock (including, among other types, many cases of cardiogenic shock- e.g., after a myocardial infarction or during heart failure; distributive shock, hypovolemic shock, resulting from large blood loss; and severe cases of septic shock)

- Heart Disease (myocardial infarction- heart attack; acute or chronic congestive or other heart failure, ruptured or dissecting aneurysms; large, especially hemorrhagic, stroke; some untreated congenital heart defects; failed heart transplant)

- Superior mesenteric artery syndrome

- Drugs that affect blood pressure

- Drinking seawater

- As a complication of dialysis

- Intoxicative inhalants

The effects of a circulatory collapse vary based on the type of collapse it is. Peripheral collapses usually involve abnormally low blood pressure and result in collapsed arteries and/or veins, leading to oxygen deprivation to tissues, organs, and limbs.

Acute collapse can result from heart failure causing the primary vessels of the heart to collapse, perhaps combined with cardiac arrest.

Particulate matter has been studied for its short- and long-term exposure effects on cardiovascular disease. Currently, PM is the major focus, in which gradients are used to determine CVD risk. For every 10 μg/m of PM long-term exposure, there was an estimated 8–18% CVD mortality risk. Women had a higher relative risk (RR) (1.42) for PM induced coronary artery disease than men (0.90) did. Overall, long-term PM exposure increased rate of atherosclerosis and inflammation. In regards to short-term exposure (2 hours), every 25 μg/m of PM resulted in a 48% increase of CVD mortality risk. In addition, after only 5 days of exposure, a rise in systolic (2.8 mmHg) and diastolic (2.7 mmHg) blood pressure occurred for every 10.5 μg/m of PM. Other research has implicated PM in irregular heart rhythm, reduced heart rate variability (decreased vagal tone), and most notably heart failure. PM is also linked to carotid artery thickening and increased risk of acute myocardial infarction.

A 2015 SBU-report looking at non-chemical factors found an association for those:

- with mentally stressful work with a lack of control over their working situation — with an effort-reward imbalance

- who experience low social support at work; who experience injustice or experience insufficient opportunities for personal development; or those who experience job insecurity

- those who work night schedules; or have long working weeks

- those who are exposed to noise

Specifically the risk of stroke was also increased by exposure to ionizing radiation. Hypertension develops more often in those who experience job strain and who have shift-work. Differences between women and men in risk are small, however men risk suffering and dying of heart attacks or stroke twice as often as women during working life.

It is most commonly caused by:

- Oesophageal rupture, for example in Boerhaave syndrome

- Asthma or other conditions leading to alveolar rupture

- Bowel rupture, where air in the abdominal cavity tracts up into the chest.

It has also been associated with:

- "Mycoplasma pneumoniae" pneumonia

- obesity

It can be induced to assist thoracoscopic surgery. It can be caused by a pulmonary barotrauma resulting when a person moves to or from a higher pressure environment, such as when a SCUBA diver, a free-diver or an airplane passenger ascends or descends.

In rare cases, pneumomediastinum may also arise as a result of blunt chest trauma (e.g. car accidents, fights, over pressure of breathing apparatus), while still evolving in the same fashion as the spontaneous form.

Pneumomediastinum is most commonly seen in otherwise healthy young male patients and may not be prefaced by a relevant medical history of similar ailments.

VALI is most common in patients receiving mechanical ventilation for acute lung injury or acute respiratory distress syndrome (ALI/ARDS).

Possible reasons for predisposition to VALI include:

- An injured lung may be at risk for further injury

- Cyclic atelectasis is particularly common in an injured lung

The annual incidence of ARDS is 13–23 people per 100,000 in the general population. Its incidence in the mechanically ventilated population in intensive care units is much higher. According to Brun-Buisson "et al" (2004), there is a prevalence of acute lung injury (ALI) of 16.1% percent in ventilated patients admitted for more than 4 hours.

Worldwide, severe sepsis is the most common trigger causing ARDS. Other triggers include mechanical ventilation, sepsis, pneumonia, Gilchrist's disease, drowning, circulatory shock, aspiration, traumaespecially pulmonary contusionmajor surgery, massive blood transfusions, smoke inhalation, drug reaction or overdose, fat emboli and reperfusion pulmonary edema after lung transplantation or pulmonary embolectomy. Pneumonia and sepsis are the most common triggers, and pneumonia is present in up to 60% of patients and may be either causes or complications of ARDS. Alcohol excess appears to increase the risk of ARDS. Diabetes was originally thought to decrease the risk of ARDS, but this has shown to be due to an increase in the risk of pulmonary edema. Elevated abdominal pressure of any cause is also probably a risk factor for the development of ARDS, particularly during mechanical ventilation.

The death rate varies from 25–40% in centers using up-to-date ventilatory strategies and up to 58% in all centers.

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.

A series of 2009 studies published in the Journal of Cardiovascular Pharmacology suggest that Metformin may prevent cardiac reperfusion injury by inhibition of Mitochondrial Complex I and the opening of MPT pore and in rats.

Since ARDS is an extremely serious condition which requires invasive forms of therapy it is not without risk. Complications to be considered include the following:

- Pulmonary: barotrauma (volutrauma), pulmonary embolism (PE), pulmonary fibrosis, ventilator-associated pneumonia (VAP)

- Gastrointestinal: bleeding (ulcer), dysmotility, pneumoperitoneum, bacterial translocation

- Cardiac: abnormal heart rhythms, myocardial dysfunction

- Kidney: acute kidney failure, positive fluid balance

- Mechanical: vascular injury, pneumothorax (by placing pulmonary artery catheter), tracheal injury/stenosis (result of intubation and/or irritation by endotracheal tube

- Nutritional: malnutrition (catabolic state), electrolyte deficiency.

A study of aortic cross-clamping, a common procedure in cardiac surgery, demonstrated a strong potential benefit with further research ongoing.

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.

A 2017 SBU report found evidence that workplace exposure to silica dust, engine exhaust or welding fumes is associated with heart disease. Associations also exist for exposure to arsenic, benzopyrenes, lead, dynamite, carbon disulphide, carbon monoxide, metalworking fluids and occupational exposure to tobacco smoke. Working with the electrolytic production of aluminium or the production of paper when the sulphate pulping process is used is associated with heart disease. An association was also found between heart disease and exposure to compounds which are no longer permitted in certain work environments, such as phenoxy acids containing TCDD(dioxin) or asbestos.

Workplace exposure to silica dust or asbestos is also associated with pulmonary heart disease. There is evidence that workplace exposure to lead, carbon disulphide, phenoxyacids containing TCDD, as well as working in an environment where aluminium is being electrolytically produced, is associated with stroke.

24 percent of all patients mechanically ventilated will develop VALI for reasons other than ALI or ARDS. The incidence is probably higher among patients who already have ALI/ARDS, but estimates vary widely. The variable estimates reflect the difficulty in distinguishing VALI from progressive ALI/ARDS.

A 2015 SBU-report including a systematic review of non-chemical riskfactors for occupation cardiovascular disease found an association between certain occupational risk factors and developing cardiovascular disease in those:

- With mentally stressfull work with a lack of control of their own working situation — with a effort-reward imbalance

- Who experience low social support at work; who experience injustice or experience insufficient opportunities for personal development; or those who experience job insecurity

- Those who work night schedules; or have long working weeks

- Those who are exposed to noise

Specifically the risk of stroke was also increased by:

- Exposure to ionizing radiation

Hypertension develops more often in those who experience job strain and who have shift-work. Differences between women and men in risk are small, however men risk suffering and dieing of heart attacks or stroke twice as often as women during working life.

The most common cause is post-surgical atelectasis, characterized by splinting, i.e. restricted breathing after abdominal surgery.

Another common cause is pulmonary tuberculosis. Smokers and the elderly are also at an increased risk. Outside of this context, atelectasis implies some blockage of a bronchiole or bronchus, which can be within the airway (foreign body, mucus plug), from the wall (tumor, usually squamous cell carcinoma) or compressing from the outside (tumor, lymph node, tubercle). Another cause is poor surfactant spreading during inspiration, causing the surface tension to be at its highest which tends to collapse smaller alveoli. Atelectasis may also occur during suction, as along with sputum, air is withdrawn from the lungs. There are several types of atelectasis according to their underlying mechanisms or the distribution of alveolar collapse; resorption, compression, microatelectasis and contraction atelectasis.

Dysbaric osteonecrosis is a significant occupational hazard, occurring in 50% of commercial Japanese divers, 65% of Hawaiian fishermen and 16% of commercial and caisson divers in the UK.

Its relationship to compressed air is strong in that it may follow a single exposure to compressed air, may occur with no history of DCS but is usually associated with significant compressed air exposure. The distribution of lesions differs with the type of exposure - the juxta-articular lesions being more common in caisson workers than in divers.

There is a definite relationship between length of time exposed to extreme depths and the percentage of divers with bone lesions. Evidence does not suggest that dysbaric osteonecrosis is a significant risk in recreational scuba diving.

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.

If the diver has not been exposed to excessive depth and decompression and presents as DON, there may be a predisposition for the condition. Diving should be restricted to shallow depths. Divers who have suffered from DON are at increased risk of future fracture of a juxta-articular lesion during a dive, and may face complications with future joint replacements. Because of the young age of the population normally affected, little data is available regarding joint replacement complications.

There is the potential for worsening of DON for any diving where there might be a need for decompression, experimental or helium diving. Physically stressful diving should probably be restricted, both in sport diving and work diving due to the possibility of unnecessary stress to the joint. Any diving should be less than 40 feet/12 meters. These risks are affected by the degree of disability and by the type of lesion (juxta-articular or shaft).

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

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 sudden cardiac deaths of 387 young American athletes (under age 35) were analyzed in a 2003 medical review:

While most causes of sudden cardiac death relate to congenital or acquired cardiovascular disease, an exception is commotio cordis, in which the heart is structurally normal but a potentially fatal loss of rhythm occurs because of the accident of timing of a blow to the chest. Its fatality rate is about 65% even with prompt CPR and defibrillation, and more than 80% without.

Age 35 serves as an approximate borderline for the likely cause of sudden cardiac death. Before age 35, congenital abnormalities of the heart and blood vessels predominate. These are usually asymptomatic prior to the fatal event, although not invariably so. Congenital cardiovascular deaths are reported to occur disproportionately in African-American athletes.

After age 35, acquired coronary artery disease predominates (80%), and this is true regardless of the athlete's former level of fitness.

Before the development of modern cardiovascular surgery, cases of acute mediastinitis usually arose from either perforation of the esophagus or from contiguous spread of odontogenic or retropharyngeal infections. However, in modern practice, most cases of acute mediastinitis result from complications of cardiovascular or endoscopic surgical procedures.

Treatment usually involves aggressive intravenous antibiotic therapy and hydration. If discrete fluid collections or grossly infected tissue have formed (such as abscesses), they may have to be surgically drained or debrided.

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.

The atmosphere is composed of 78% nitrogen and 21% oxygen. Since oxygen is exchanged at the alveoli-capillary membrane, nitrogen is a major component for the alveoli's state of inflation. If a large volume of nitrogen in the lungs is replaced with oxygen, the oxygen may subsequently be absorbed into the blood, reducing the volume of the alveoli, resulting in a form of alveolar collapse known as absorption atelectasis.