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.

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.

The presentation of shock is variable with some people having only minimal symptoms such as confusion and weakness. While the general signs for all types of shock are low blood pressure, decreased urine output, and confusion, these may not always be present. While a fast heart rate is common, those on β-blockers, those who are athletic and in 30% of cases of those with shock due to intra abdominal bleeding may have a normal or slow heart rate. Specific subtypes of shock may have additional symptoms.

Symptoms of cardiogenic shock include:

- Distended jugular veins due to increased jugular venous pressure

- Weak or absent pulse

- Abnormal heart rhythms, often a fast heart rate

- Pulsus paradoxus in case of tamponade

- Reduced blood pressure

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.

Septic shock is a serious medical condition that occurs when sepsis, which is organ injury or damage in response to infection, leads to dangerously low blood pressure and abnormalities in cellular metabolism.

The primary infection is most commonly caused by bacteria, but also may be by fungi, viruses or parasites. It may be located in any part of the body, but most commonly in the lungs, brain, urinary tract, skin or abdominal organs. It can cause multiple organ dysfunction syndrome (formerly known as multiple organ failure) and death.

Frequently, people with septic shock are cared for in intensive care units. It most commonly affects children, immunocompromised individuals, and the elderly, as their immune systems cannot deal with infection so effectively as those of healthy adults. The mortality rate from septic shock is approximately 25–50%.

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.

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.

Electrical injury is a physiological reaction caused by electric current passing through the (human) body. Electric shock occurs upon contact of a (human) body part with any source of electricity that causes a sufficient magnitude of current to pass through the victim's flesh, viscera or hair. Physical contact with energized wiring or devices is the most common cause of an electric shock. In cases of exposure to high voltages, such as on a power transmission tower, physical contact with energized wiring or objects may not be necessary to cause electric shock, as the voltage may be sufficient to "jump" the air gap between the electrical device and the victim.

The injury related to electric shock depends on the magnitude of the current. Very small currents may be imperceptible or produce a light tingling sensation. A shock caused by low current that would normally be harmless could startle an individual and cause injury due to suddenly jerking away from the source of electricity, resulting in one striking a stationary object, dropping an object being held or falling. Stronger currents may cause some degree of discomfort or pain, while more intense currents may induce involuntary muscle contractions, preventing the victim from breaking free of the source of electricity. Still larger currents usually result in tissue damage and may trigger fibrillation of the heart or cardiac arrest, any of which may ultimately be fatal. If death results from an electric shock the cause of death is generally referred to as electrocution.

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.

Clinical symptoms may not be present until 10–20% of total whole-blood volume is lost.

Hypovolemia can be recognized by tachycardia, diminished blood pressure, and the absence of perfusion as assessed by skin signs (skin turning pale) and/or capillary refill on forehead, lips and nail beds. The patient may feel dizzy, faint, nauseated, or very thirsty. These signs are also characteristic of most types of shock.

Note that in children compensation can result in an artificially high blood pressure despite hypovolemia. Children will typically compensate (maintain blood pressure despite loss of blood volume) for a longer period than adults, but will deteriorate rapidly and severely once they do begin to decompensate. This is another reason (aside from initial lower blood volume) that even the possibility of internal bleeding in children should almost always be treated aggressively.

Obvious signs of external bleeding should be noted while remembering that people can bleed to death internally without any external blood loss. ("Blood on the floor, plus 4 more" = intrathoracic, intraperitoneal, retroperitoneal, pelvis/thigh)

There should be considered possible mechanisms of injury that may have caused internal bleeding, such as ruptured or bruised internal organs. If trained to do so and if the situation permits, there should be conducted a secondary survey and checked the chest and abdomen for pain, deformity, guarding, discoloration or swelling. Bleeding into the abdominal cavity can cause the classical bruising patterns of Grey Turner's sign or Cullen's sign.

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.

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.

Symptoms of toxic shock syndrome vary depending on the underlying cause. TSS resulting from infection with the bacterium "Staphylococcus aureus" typically manifests in otherwise healthy individuals via signs and symptoms including high fever, accompanied by low blood pressure, malaise and confusion, which can rapidly progress to stupor, coma, and multiple organ failure. The characteristic rash, often seen early in the course of illness, resembles a sunburn, and can involve any region of the body including the lips, mouth, eyes, palms and soles. In patients who survive the initial phase of the infection, the rash desquamates, or peels off, after 10–14 days.

In contrast, TSS caused by the bacterium "Streptococcus pyogenes", or TSLS, typically presents in people with pre-existing skin infections with the bacteria. These individuals often experience severe pain at the site of the skin infection, followed by rapid progression of symptoms as described above for TSS. In contrast to TSS caused by "Staphylococcus", streptococcal TSS less often involves a sunburn-like rash.

Spinal shock was first defined by Whytt in 1750 as a loss of accompanied by motor paralysis with initial loss but gradual recovery of reflexes, following a spinal cord injury (SCI) – most often a complete transection. Reflexes in the spinal cord below the level of injury are depressed (hyporeflexia) or absent (areflexia), while those above the level of the injury remain unaffected. The 'shock' in spinal shock does not refer to circulatory collapse, and should not be confused with neurogenic shock, which is life-threatening

In spinal cord injuries above T6, neurogenic shock may occur, from the loss of autonomic innervation from the brain. Parasympathetic is preserved but the synergy between sympathetic and parasympathetic system is lost in cervical and high thoracic SCI lesions. Sacral parasympathetic loss may be encountered in lesions below T6 or T7. Cervical lesions cause total loss of sympathetic innervation and lead to vasovagal hypotension and bradyarrhythmias – which resolve in 3–6 weeks. Autonomic dysreflexia is permanent, and occurs from Phase 4 onwards. It is characterized by unchecked sympathetic stimulation below the SCI (from a loss of cranial regulation), leading to often extreme hypertension, loss of bladder or bowel control, sweating, headaches, and other sympathetic effects.

An electrocardiogram helps establishing the exact diagnosis and guides treatment, it may reveal:

- Abnormal heart rhythms, such as bradycardia (slowed heart rate)

- myocardial infarction (ST-elevation MI, STEMI, is usually more dangerous than non-STEMIs; MIs that affect the ventricles are usually more dangerous than those that affect the atria; those affecting the left side of the heart, especially the left ventricle, are usually more dangerous than those affecting the right side, unless that side is severely compromised)

- Signs of cardiomyopathy

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.

First symptoms may be subtle such as mild pain, flank tenderness, haematuria. Depending on blood loss, symptoms of hypovolemic shock may develop. Hematoma is usually contained in the retroperitoneum, allowing for a period of haemodynamic stability. Sometimes massive acute hemorrhage is seen when a hematoma ruptures Gerota's fascia and extends into the peritoneum. An ultrasound or CT scan can establish diagnosis, while lab tests may be inconclusive as changes of haematocrit or haemoglobin are not specific to the syndrome, while haematuria is not always present.

Tachycardia is often asymptomatic. If the heart rate is too high, cardiac output may fall due to the markedly reduced ventricular filling time. Rapid rates, though they may be compensating for ischemia elsewhere, increase myocardial oxygen demand and reduce coronary blood flow, thus precipitating an ischemic heart or valvular disease. Sinus tachycardia accompanying a myocardial infarction may be indicative of cardiogenic shock.

Usually in women with no heart problems, this syndrome is characterized by normal resting heart rate but exaggerated postural sinus tachycardia with or without orthostatic hypotension.

Claudication is a medical term usually referring to impairment in walking, or pain, discomfort, numbness, or tiredness in the legs that occurs during walking or standing and is relieved by rest. The perceived level of pain from claudication can be mild to extremely severe. Claudication is most common in the calves but it can also affect the feet, thighs, hips, buttocks, or arms. The word "claudication" comes from the Latin "claudicare" meaning 'to limp'.

Claudication that appears after a short amount of walking may sometimes be described by US medical professionals by the number of typical city street blocks that the patient can walk before the onset of claudication. Thus, "one-block claudication" appears after walking one block, "two-block claudication" appears after walking two blocks, etc. The term "block" would be understood more exactly locally but is on the order of 100 metres.

Toxic shock syndrome (TSS) is a condition caused by bacterial toxins. Symptoms may include fever, rash, skin peeling, and low blood pressure. There may also be symptoms related to the specific underlying infection such as mastitis, osteomyelitis, necrotising fasciitis, or pneumonia.

TSS is caused by bacteria of either the "Streptococcus pyogenes" or "Staphylococcus aureus" type. Streptococcal toxic shock syndrome (STSS) is sometimes referred to as toxic shock-like syndrome (TSLS). The underlying mechanism involves the production of superantigens during an invasive streptococcus infection or a localized staphylococcus infection. Risk factors for the staphylococcal type include the use of very absorbent tampons and skin lesions in young children. Diagnosis is typically based on symptoms.

Treatment includes antibiotics, incision and drainage of any abscesses, and possibly intravenous immunoglobulin. The need for rapid removal of infected tissue via surgery in those with a streptococcal cause while commonly recommended is poorly supported by the evidence. Some recommend delaying surgical debridement. The overall risk of death in streptococcal disease is about 50% while in staphylococcal disease it is around 5%. Death may occur within 2 days.

In the United States streptococcal TSS occurs in about 3 per 100,000 per year while staphylococcal TSS occurs in about 0.5 per 100,000 per year. The condition is more common in the developing world. It was first described in 1927. Due to the association with very absorbent tampons, these products were removed from sale.