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.

Based on endocrine disturbances such as:

- Hypothyroidism (can be considered a form of cardiogenic shock) in critically ill patients, reduces cardiac output and can lead to hypotension and respiratory insufficiency.

- Thyrotoxicosis (cardiogenic shock) may induce a reversible cardiomyopathy.

- Acute adrenal insufficiency (distributive shock) is frequently the result of discontinuing corticosteroid treatment without tapering the dosage. However, surgery and intercurrent disease in patients on corticosteroid therapy without adjusting the dosage to accommodate for increased requirements may also result in this condition.

- Relative adrenal insufficiency (distributive shock) in critically ill patients where present hormone levels are insufficient to meet the higher demands

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.

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.

Septic shock is associated with significant mortality and is the leading non cardiac cause of death in intensive care units (ICUs).

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.

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.

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.

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

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.

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.

Low blood pressure can be caused by low blood volume, hormonal changes, widening of blood vessels, medicine side effects, anemia, heart problems or endocrine problems.

Reduced blood volume, hypovolemia, is the most common cause of hypotension. This can result from hemorrhage; insufficient fluid intake, as in starvation; or excessive fluid losses from diarrhea or vomiting. Hypovolemia is often induced by excessive use of diuretics. Low blood pressure may also be attributed to heat stroke. The body may have enough fluid but does not retain electrolytes. Absence of perspiration, light headedness and dark coloured urine are also indicators.

Other medications can produce hypotension by different mechanisms. Chronic use of alpha blockers or beta blockers can lead to hypotension. Beta blockers can cause hypotension both by slowing the heart rate and by decreasing the pumping ability of the heart muscle.

Decreased cardiac output despite normal blood volume, due to severe congestive heart failure, large myocardial infarction, heart valve problems, or extremely low heart rate (bradycardia), often produces hypotension and can rapidly progress to cardiogenic shock. Arrhythmias often result in hypotension by this mechanism.

Some heart conditions can lead to low blood pressure, including extremely low heart rate (bradycardia), heart valve problems, heart attack and heart failure. These conditions may cause low blood pressure because they prevent the body from being able to circulate enough blood.

Excessive vasodilation, or insufficient constriction of the resistance blood vessels (mostly arterioles), causes hypotension. This can be due to decreased sympathetic nervous system output or to increased parasympathetic activity occurring as a consequence of injury to the brain or spinal cord or of dysautonomia, an intrinsic abnormality in autonomic system functioning. Excessive vasodilation can also result from sepsis, acidosis, or medications, such as nitrate preparations, calcium channel blockers, or AT1 receptor antagonists (Angiotensin II acts on AT1 receptors). Many anesthetic agents and techniques, including spinal anesthesia and most inhalational agents, produce significant vasodilation.

Meditation, yoga, or other mental-physiological disciplines may reduce hypotensive effects.

Lower blood pressure is a side effect of certain herbal medicines, which can also interact with hypotensive medications. An example is the theobromine in "Theobroma cacao", which lowers blood pressure through its actions as both a vasodilator and a diuretic, and has been used to treat high blood pressure.

Hypotension is low blood pressure, especially in the arteries of the systemic circulation. Blood pressure is the force of blood pushing against the walls of the arteries as the heart pumps out blood. A systolic blood pressure of less than 90 millimeters of mercury (mm Hg) or diastolic of less than 60 mm Hg is generally considered to be hypotension. However, in practice, blood pressure is considered too low only if noticeable symptoms are present.

Hypotension is the opposite of hypertension, which is high blood pressure. It is best understood as a physiological state, rather than a disease. Severely low blood pressure can deprive the brain and other vital organs of oxygen and nutrients, leading to a life-threatening condition called shock.

For some people who exercise and are in top physical condition, low blood pressure is a sign of good health and fitness.

For many people, excessively low blood pressure can cause dizziness and fainting or indicate serious heart, endocrine or neurological disorders.

Treatment of hypotension may include the use of intravenous fluids or vasopressors. When using vasopressors, trying to achieve a mean arterial pressure (MAP) of greater than 70 mmHg does not appear to result in better outcomes than trying to achieve a MAP of greater than 65 mm Hg in adults.

The lethality of an electric shock is dependent on several variables:

- Current. The higher the current, the more likely it is lethal. Since current is proportional to voltage when resistance is fixed (ohm's law), high voltage is an indirect risk for producing higher currents.

- Duration. The longer the duration, the more likely it is lethal—safety switches may limit time of current flow

- Pathway. If current flows through the heart muscle, it is more likely to be lethal.

- High voltage (over about 600 volts). In addition to greater current flow, high voltage may cause dielectric breakdown at the skin, thus lowering skin resistance and allowing further increased current flow.

- medical implants. Artificial cardiac pacemakers or implantable cardioverter-defibrillators (ICD) are sensitive to very small currents.

- pre-existing medical condition.

- Age and Sex.

Other issues affecting lethality are frequency, which is an issue in causing cardiac arrest or muscular spasms. Very high frequency electric current causes tissue burning, but does not penetrate the body far enough to cause cardiac arrest (see electrosurgery). Also important is the pathway: if the current passes through the chest or head, there is an increased chance of death. From a main circuit or power distribution panel the damage is more likely to be internal, leading to cardiac arrest. Another factor is that cardiac tissue has a chronaxie (response time) of about 3 milliseconds, so electricity at frequencies of higher than about 333 Hz requires more current to cause fibrillation than is required at lower frequencies.

The comparison between the dangers of alternating current at typical power transmission frequences (i.e., 50 or 60 Hz), and direct current has been a subject of debate ever since the War of Currents in the 1880s. Animal experiments conducted during this time suggested that alternating current was about twice as dangerous as direct current per unit of current flow (or per unit of applied voltage).

It is sometimes suggested that human lethality is most common with alternating current at 100–250 volts; however, death has occurred below this range, with supplies as low as 42 volts. Assuming a steady current flow (as opposed to a shock from a capacitor or from static electricity), shocks above 2,700 volts are often fatal, with those above 11,000 volts being usually fatal, though exceptional cases have been noted. According to a Guinness Book of World Records comic, seventeen-year-old Brian Latasa survived a 230,000 volt shock on the tower of an ultra-high voltage line in Griffith Park, Los Angeles on November 9, 1967. A news report of the event stated that he was "jolted through the air, and landed across the line", and though rescued by firemen, he suffered burns over 40% of his body and was completely paralyzed except for his eyelids.

Heating due to resistance can cause extensive and deep burns. Voltage levels of 500 to 1000 volts tend to cause internal burns due to the large energy (which is proportional to the duration multiplied by the square of the voltage divided by resistance) available from the source. Damage due to current is through tissue heating. For most cases of high-energy electrical trauma, the Joule heating in the deeper tissues along the extremity will reach damaging temperatures in a few seconds.

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

In mostly European experience with 69 patients during 1996-2016, the 5- and 10-year survival rates for SCLS patients were 78% and 69%, respectively, but the survivors received significantly more frequent preventive treatment with IVIG than did non-survivors. Five- and 10-year survival rates in patients treated with IVIG were 91% and 77%, respectively, compared to 47% and 37% in patients not treated with IVIG. Moreover, better identification and management of this condition appears to be resulting in lower mortality and improving survival and quality-of-life results as of late.

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.

Traumatic cardiac arrest (TCA) is a condition in which the heart has ceased to beat due to blunt or penetrating trauma, such as a stab wound to the thoracic area. It is a medical emergency which will always result in death without prompt advanced medical care. Even with prompt medical intervention, survival without neurological complications is rare. There are no definitive protocols in place in how to manage traumatic cardiac arrest, but certain people benefit from the use of a thoracotomy in order to gain access and repair damage from the injury. Traumatic cardiac arrest is a complex form of cardiac arrest often derailing from Advanced Cardiac Life Support in the sense that the emergency team must first establish the cause of the traumatic arrest and reverse these effects, for example hypovolemia and haemorrhagic shock due to a penetrating injury.

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.

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.

The initial stage is the capillary leak phase, lasting from 1 to 3 days, during which up to 70% of total plasma volume may invade cavities especially in the extremities. The most common clinical features are flu-like symptoms such as fatigue; runny nose; lightheadedness up to and including syncope (fainting); limb, abdominal or generalized pain; facial or other edema; dyspnea; and hypotension that results in circulatory shock and potentially in cardiopulmonary collapse and other organ distress or damage. Acute renal dysfunction or failure is a common risk due to acute tubular necrosis consequent to hypovolemia and rhabdomyolysis.

The loss of fluid out of the capillaries has similar effects on the circulation as dehydration, slowing both the flow of oxygen delivered to tissues and organs as well as the output of urine. Urgent medical attention in this phase consists of fluid resuscitation efforts, mainly the intravenous administration of saline solution plus hetastarch or albumin and colloids (to increase the remaining blood flow to vital organs like the kidneys), as well as glucocorticoids (steroids like methylprednisolone, to reduce or stop the capillary leak). However effective on blood pressure, the impact of fluid therapy is always transient and leads to increased extravascular fluid accumulation, engendering multiple complications especially compartment syndrome and thus limb-destructive rhabdomyolysis. Consequently, patients experiencing episodes of SCLS should be closely monitored in a hospital intensive-care setting, including for orthopedic complications requiring surgical decompression, and their fluid therapy should be minimized as much as possible.

Non-occlusive disease has a poor prognosis with survival rate between 40-50%.