Haemorrhagic shock occurs in about 1–2% of trauma cases. Up to one-third of people admitted to the intensive care unit (ICU) are in circulatory shock.

Distributive shock is due to impaired utilization of oxygen and thus production of energy by the cell. Examples of this form of shock are:

- Septic shock is the most common cause of distributive shock. Caused by an overwhelming systemic infection resulting in vasodilation leading to hypotension. Septic shock can be caused by Gram negative bacteria such as (among others) "Escherichia coli", Proteus species, "Klebsiella pneumoniae" which have an endotoxin on their surface which produces adverse biochemical, immunological and occasionally neurological effects which are harmful to the body, and other Gram-positive cocci, such as pneumococci and streptococci, and certain fungi as well as Gram-positive bacterial toxins. Septic shock also includes some elements of cardiogenic shock. In 1992, the ACCP/SCCM Consensus Conference Committee defined septic shock: ". . .sepsis-induced hypotension (systolic blood pressure < 90 mmHg or a reduction of 40 mmHg from baseline) despite adequate fluid resuscitation along with the presence of perfusion abnormalities that may include, but are not limited to, lactic acidosis, oliguria, or an acute alteration in mental status. Patients who are receiving inotropic or vasopressor agents may have a normalized blood pressure at the time that perfusion abnormalities are identified."

- Anaphylactic shock is caused by a severe anaphylactic reaction to an allergen, antigen, drug or foreign protein causing the release of histamine which causes widespread vasodilation, leading to hypotension and increased capillary permeability.

- High spinal injuries may cause neurogenic shock. The classic symptoms include a slow heartrate due to loss of cardiac sympathetic tone and warm skin due to dilation of the peripheral blood vessels. (This term can be confused with spinal shock which is a recoverable loss of function of the spinal cord after injury and does not refer to the haemodynamic instability per se.)

Septic shock is a result of a systemic response to infection or multiple infectious causes. Sepsis may be present, but septic shock may occur without it. The precipitating infections that may lead to septic shock if severe enough include but are not limited to appendicitis, pneumonia, bacteremia, diverticulitis, pyelonephritis, meningitis, pancreatitis, necrotizing fasciitis, MRSA and mesenteric ischemia.

Sepsis is a constellation of symptoms secondary to an infection that manifests as disruptions in heart rate, respiratory rate, temperature, and white blood cell count. If sepsis worsens to the point of end-organ dysfunction (kidney failure, liver dysfunction, altered mental status, or heart damage), then the condition is called severe sepsis. Once severe sepsis worsens to the point where blood pressure can no longer be maintained with intravenous fluids alone, then the criterion has been met for septic shock.

Septic shock is a subclass of distributive shock, a condition in which abnormal distribution of blood flow in the smallest blood vessels results in inadequate blood supply to the body tissues, resulting in ischemia and organ dysfunction. Septic shock refers specifically to distributive shock due to sepsis as a result of infection.

Septic shock may be defined as sepsis-induced low blood pressure that persists despite treatment with intravenous fluids. Low blood pressure reduces tissue perfusion pressure, causing the tissue hypoxia that is characteristic of shock. Cytokines released in a large scale inflammatory response result in massive vasodilation, increased capillary permeability, decreased systemic vascular resistance, and low blood pressure. Finally, in an attempt to offset decreased blood pressure, ventricular dilatation and myocardial dysfunction occur.

Septic shock may be regarded as a stage of SIRS (Systemic Inflammatory Response Syndrome), in which sepsis, severe sepsis and multiple organ dysfunction syndrome (MODS) represent different stages of a pathophysiological process. If an organism cannot cope with an infection, it may lead to a systemic response - sepsis, which may further progress to severe sepsis, septic shock, organ failure, and eventually, result in death.

In addition to sepsis, distributive shock can be caused by systemic inflammatory response syndrome (SIRS) due to conditions other than infection such as pancreatitis, burns or trauma. Other causes include, toxic shock syndrome (TSS), anaphylaxis (a sudden, severe allergic reaction), adrenal insufficiency, reactions to drugs or toxins, heavy metal poisoning, hepatic (liver) insufficiency and damage to the central nervous system. Causes of adrenal insufficiency leading to distributive shock include acute worsening of chronic adrenal insufficiency, destruction or removal of the adrenal glands, suppression of adrenal gland function due to exogenous steroids, hypopituitarism and metabolic failure of hormone production.

Distributive shock is a medical condition in which abnormal distribution of blood flow in the smallest blood vessels results in inadequate supply of blood to the body's tissues and organs. It is one of four categories of shock, a condition where there is not enough oxygen-carrying blood to meet the metabolic needs of the cells which make up the body's tissues and organs. Distributive shock is different from the other three categories of shock in that it occurs even though the output of the heart is at or above a normal level. The most common cause is sepsis leading to type of distributive shock called septic shock, a condition that can be fatal.

Neurogenic shock is a distributive type of shock resulting in low blood pressure, occasionally with a slowed heart rate, that is attributed to the disruption of the autonomic pathways within the spinal cord. It can occur after damage to the central nervous system such as spinal cord injury. Low blood pressure occurs due to decreased systemic vascular resistance resulting in pooling of blood within the extremities lacking sympathetic tone. The slowed heart rate results from unopposed vagal activity and has been found to be exacerbated by hypoxia and endobronchial suction.

Neurogenic shock can be a potentially devastating complication, leading to organ dysfunction and death if not promptly recognized and treated. It is not to be confused with spinal shock, which is not circulatory in nature.

OSHA found that up to 80 percent of its electrical injuries involve thermal burns due to arcing faults. The arc flash in an electrical fault produces the same type of light radiation from which electric welders protect themselves using face shields with dark glass, heavy leather gloves, and full-coverage clothing. The heat produced may cause severe burns, especially on unprotected flesh. The arc blast produced by vaporizing metallic components can break bones and damage internal organs. The degree of hazard present at a particular location can be determined by a detailed analysis of the electrical system, and appropriate protection worn if the electrical work must be performed with the electricity on.

A domestic power supply voltage (110 or 230 V), 50 or 60 Hz alternating current (AC) through the chest for a fraction of a second may induce ventricular fibrillation at currents as low as . With direct current (DC), 300 to 500 mA is required. If the current has a direct pathway to the heart (e.g., via a cardiac catheter or other kind of electrode), a much lower current of less than 1 mA (AC or DC) can cause fibrillation. If not immediately treated by defibrillation, fibrillation is usually lethal because all of the heart muscle fibres move independently instead of in the coordinated pulses needed to pump blood and maintain circulation. Above 200 mA, muscle contractions are so strong that the heart muscles cannot move at all, but these conditions prevent fibrillation.

Neurogenic shock can result from severe central nervous system damage (brain injury, cervical or high thoracic spinal cord). In more simple terms: the trauma causes a sudden loss of background sympathetic stimulation to the blood vessels. This causes them to relax (vasodilation) resulting in a sudden decrease in blood pressure (secondary to a decrease in peripheral vascular resistance).

Neurogenic shock results from damage to the spinal cord above the level of the 6th thoracic vertebra. It is found in about half of people who suffer spinal cord injury within the first 24 hours, and usually doesn't go away for one to three weeks.

Surgical shock is the shock to the circulation resulting from surgery. It is commonly due to a loss of blood which results in insufficient blood volume.

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.

With proper treatment, people usually recover in two to three weeks. The condition can, however, be fatal within hours.

Cardiogenic shock is caused by the failure of the heart to pump effectively. It can be due to damage to the heart muscle, most often from a large myocardial infarction. Other causes include abnormal heart rhythms, cardiomyopathy, heart valve problems, ventricular outflow obstruction (i.e. aortic valve stenosis, aortic dissection, cardiac tamponade, constrictive pericarditis, systolic anterior motion (SAM) in hypertrophic cardiomyopathy), or ventriculoseptal defects.

It can also be caused by a sudden decompressurization (e.g. in an aircraft), where air bubbles are released into the bloodstream (Henry's Law), causing heart failure.

Cardiogenic shock is a life-threatening medical condition resulting from an inadequate circulation of blood due to primary failure of the ventricles of the heart to function effectively. Signs of inadequate blood flow to the body's organs include low urine production (<30 mL/hour), cool arms and legs, and altered level of consciousness. It may lead to cardiac arrest, which is an abrupt stopping of cardiac pump function.

As this is a type of circulatory shock, there is insufficient blood flow and oxygen supply for biological tissues to meet the metabolic demands for oxygen and nutrients. Cardiogenic shock is defined by sustained low blood pressure with tissue hypoperfusion despite adequate left ventricular filling pressure.

Treatment of cardiogenic shock depends on the cause. If cardiogenic shock is due to a heart attack, attempts to open the heart's arteries may help. An intra-aortic balloon pump or left ventricular assist device may improve matters until this can be done. Medications that improve the heart's ability to contract (positive inotropes) may help; however, it is unclear which is best. Norepinephrine may be better if the blood pressure is very low whereas dopamine or dobutamine may be more useful if only slightly low. Cardiogenic shock is a condition that is difficult to fully reverse even with an early diagnosis. With that being said, early initiation of mechanical circulatory support, early percutaneous coronary intervention, inotropes, and heart transplantation may improved outcomes.

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

Hypovolemia is a state of decreased blood volume; more specifically, decrease in volume of blood plasma. It is thus the intravascular component of volume contraction (or loss of blood volume due to things such as bleeding or dehydration), but, as it also is the most essential one, "hypovolemia" and volume contraction are sometimes used synonymously.

Hypovolemia is characterized by sodium depletion (salt depletion) and thus differs from dehydration, which is defined as excessive loss of body water.

Sinus tachycardia is usually a response to normal physiological situations, such as exercise and an increased sympathetic tone with increased catecholamine release—stress, fright, flight, anger. Other causes include:

- Pain

- Fever

- Anxiety

- Dehydration

- Malignant hyperthermia

- Hypovolemia with hypotension and shock

- Anemia

- Heart failure

- Hyperthyroidism

- Mercury poisoning

- Kawasaki disease

- Pheochromocytoma

- Sepsis

- Pulmonary embolism

- Acute coronary ischemia and myocardial infarction

- Chronic obstructive pulmonary disease

- Hypoxia

- Intake of stimulants such as caffeine, theophylline, nicotine, cocaine, or amphetamines

- Hyperdynamic circulation

- Electric shock

- Drug withdrawal

- Porphyria

- Acute inflammatory demyelinating polyradiculoneuropathy

- Postural orthostatic tachycardia syndrome

Common causes of hypovolemia are

- Loss of blood (external or internal bleeding or blood donation)

- Loss of plasma (severe burns and lesions discharging fluid)

- Loss of body sodium and consequent intravascular water; e.g. diarrhea or vomiting

Excessive sweating is not a cause of hypovolemia, because the body eliminates significantly more water than sodium.

The severity of this disease frequently warrants hospitalization. Admission to the intensive care unit is often necessary for supportive care (for aggressive fluid management, ventilation, renal replacement therapy and inotropic support), particularly in the case of multiple organ failure. The source of infection should be removed or drained if possible: abscesses and collections should be drained. Anyone wearing a tampon at the onset of symptoms should remove it immediately. Outcomes are poorer in patients who do not have the source of infection removed.

Antibiotic treatment should cover both "S. pyogenes" and "S. aureus". This may include a combination of cephalosporins, penicillins or vancomycin. The addition of clindamycin or gentamicin reduces toxin production and mortality.

Cardiac tamponade is caused by a large or uncontrolled pericardial effusion, i.e. the buildup of fluid inside the pericardium. This commonly occurs as a result of chest trauma (both blunt and penetrating), but can also be caused by myocardial rupture, cancer, uremia, pericarditis, or cardiac surgery, and rarely occurs during retrograde aortic dissection, or while the person is taking anticoagulant therapy. The effusion can occur rapidly (as in the case of trauma or myocardial rupture), or over a more gradual period of time (as in cancer). The fluid involved is often blood, but pus is also found in some circumstances.

Causes of increased pericardial effusion include hypothyroidism, physical trauma (either penetrating trauma involving the pericardium or blunt chest trauma), pericarditis (inflammation of the pericardium), iatrogenic trauma (during an invasive procedure), and myocardial rupture.

Not required for physiologic sinus tachycardia. Underlying causes are treated if present.

Acute myocardial infarction. Sinus tachycardia can present in more than a third of the patients with AMI but this usually decreases over time. Patients with sustained sinus tachycardia reflects a larger infarct that are more anterior with prominent left ventricular dysfunction, associated with high mortality and morbidity. Tachycardia in the presence of AMI can reduce coronary blood flow and increase myocardial oxygen demand, aggravating the situation. Beta blockers can be used to slow the rate, but most patients are usually already treated with beta blockers as a routine regimen for AMI.

Practically, many studies showed that there is no need for any treatment.

IST and POTS. Beta blockers are useful if the cause is sympathetic overactivity. If the cause is due to decreased vagal activity, it is usually hard to treat and one may consider radiofrequency catheter ablation.

One of the most common settings for cardiac tamponade is in the first 24 to 48 hours after heart surgery. After heart surgery, chest tubes are placed to drain blood. These chest tubes, however, are prone to clot formation. When a chest tube becomes occluded or clogged, the blood that should be drained can accumulate around the heart, leading to tamponade.

Myocardial infarction complications may occur immediately following a heart attack (in the acute phase), or may need time to develop (a chronic problem). After an infarction, an obvious complication is a second infarction, which may occur in the domain of another atherosclerotic coronary artery, or in the same zone if there are any live cells left in the infarct.

A complication that may occur in the acute setting soon after a myocardial infarction or in the weeks following is cardiogenic shock. Cardiogenic shock is defined as a hemodynamic state in which the heart cannot produce enough of a cardiac output to supply an adequate amount of oxygenated blood to the tissues of the body.

While the data on performing interventions on individuals with cardiogenic shock is sparse, trial data suggests a long-term mortality benefit in undergoing revascularization if the individual is less than 75 years old and if the onset of the acute myocardial infarction is less than 36 hours and the onset of cardiogenic shock is less than 18 hours. If the patient with cardiogenic shock is not going to be revascularized, aggressive hemodynamic support is warranted, with insertion of an intra-aortic balloon pump if not contraindicated. If diagnostic coronary angiography does not reveal a culprit blockage that is the cause of the cardiogenic shock, the prognosis is poor.