The first changes seen in shock is an increased cardiac output followed by a decrease in mixed venous oxygen saturation (SmvO2) as measured in the pulmonary artery via a pulmonary artery catheter. Central venous oxygen saturation (ScvO2) as measured via a central line correlates well with SmvO2 and are easier to acquire. If shock progresses anaerobic metabolism will begin to occur with an increased blood lactic acid as the result. While many laboratory tests are typically performed there is no test that either makes or excludes the diagnosis. A chest X-ray or emergency department ultrasound may be useful to determine volume state.

The best evidence exists for the treatment of septic shock in adults and as the pathophysiology appears similar in children and other types of shock treatment this has been extrapolated to these areas. Management may include securing the airway via intubation if necessary to decrease the work of breathing and for guarding against respiratory arrest. Oxygen supplementation, intravenous fluids, passive leg raising (not Trendelenburg position) should be started and blood transfusions added if blood loss is severe. It is important to keep the person warm as well as adequately manage pain and anxiety as these can increase oxygen consumption.

According to current guidelines, requirements for diagnosis with sepsis are "the presence (probable or documented) of infection together with systemic manifestations of infection". These manifestations may include:

- Tachypnea (fast rate of breathing), which is defined as more than 20 breaths per minute, or when testing blood gas, a less than 32 mmHg, which signifies hyperventilation

- White blood cell count either significantly low ( 12000 cells/mm)

- Tachycardia (rapid heart rate), which in sepsis is defined as a rate greater than 90 beats per minute

- Altered body temperature: Fever > or hypothermia <

Documented evidence of infection, may include positive blood culture, signs of pneumonia on chest x-ray, or other radiologic or laboratory evidence of infection. Signs of end-organ dysfunction are present in septic shock, including kidney failure, liver dysfunction, changes in mental status, or elevated serum lactate.

Septic shock is diagnosed if there is low blood pressure (BP) that does not respond to treatment. This means that intravenous fluid administration alone is not enough to maintain a patient's BP. Diagnosis of septic shock is made when systolic blood pressure is less than 90mm Hg, a mean arterial pressure (MAP) is less than 70 mm Hg, or a systolic BP decreases 40 mm Hg or more without other causes for low BP.

Because lowered blood pressure in septic shock contributes to poor perfusion, fluid resuscitation is an initial treatment to increase blood volume. Crystalloids such as normal saline and lactated Ringer's solution are recommended as the initial fluid of choice, while the use of colloid solutions such as hydroxyethyl starch have not shown any advantage or decrease in mortality. When large quantities of fluids are given, administering albumin has shown some benefit.

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 main goals of treatment in distributive shock are to reverse the underlying cause and achieve hemodynamic stabilization. Immediate treatment involves fluid resuscitation and the use of vasoactive drugs, both vasopressors and inotropes. Hydrocortisone is used for patients whose hypotension does not respond to fluid resuscitation and vasopressors. Opening and keeping open the microcirculation is a consideration in the treatment of distributive shock, as a result limiting the use of vasopressors has been suggested. Control of inflammation, vascular function and coagulation to correct pathological differences in blood flow and microvascular shunting has been pointed to as a potentially important adjunct goal in the treatment of distributive shock.

Patients with septic shock are treated with antimicrobial drugs to treat the causative infection. Some sources of infection require surgical intervention including necrotizing fasciitis, cholangitis, abscess, intestinal ischemia, or infected medical devices.

Anaphylactic shock is treated with epinephrine.

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

When cardiomyopathy is suspected as the cause of cardiogenic shock, a biopsy of heart muscle may be needed to make a definite diagnosis.

The Swan-Ganz catheter or pulmonary artery catheter may assist in the diagnosis by providing information on the hemodynamics.

For staphylococcal toxic shock syndrome, the diagnosis is based strictly upon CDC criteria defined in 2011, as follows:

1. Body temperature > 38.9 °C (102.02 °F)

2. Systolic blood pressure < 90 mmHg

3. Diffuse macular erythroderma

4. Desquamation (especially of the palms and soles) 1–2 weeks after onset

5. Involvement of three or more organ systems:

- Gastrointestinal (vomiting, diarrhea)

- Muscular: severe myalgia or creatine phosphokinase level at least twice the upper limit of normal for laboratory

- Mucous membrane hyperemia (vaginal, oral, conjunctival)

- Kidney failure (serum creatinine > 2 times normal)

- Liver inflammation (bilirubin, AST, or ALT > 2 times normal)

- Low platelet count (platelet count < 100,000 / mm)

- Central nervous system involvement (confusion without any focal neurological findings)

6. Negative results of:

- Blood, throat, and CSF cultures for other bacteria (besides "S. aureus")

- Negative serology for "Rickettsia" infection, leptospirosis, and measles

Cases are classified as confirmed or probable based on:

- Confirmed: All six of the criteria above are met (unless the patient dies before desquamation can occur)

- Probable: Five of the six criteria above are met

Emergency oxygen should be immediately employed to increase the efficiency of the patient's remaining blood supply. This intervention can be life-saving.

The use of intravenous fluids (IVs) may help compensate for lost fluid volume, but IV fluids cannot carry oxygen in the way that blood can; however, blood substitutes are being developed which can. Infusion of colloid or crystalloid IV fluids will also dilute clotting factors within the blood, increasing the risk of bleeding. It is current best practice to allow permissive hypotension in patients suffering from hypovolemic shock, both to ensure clotting factors are not overly diluted and also to stop blood pressure being artificially raised to a point where it "blows off" clots that have formed.

Usually referred to as a "class" of shock.

Most sources state that there are 4 stages of hypovolemic shock; however, a number of other systems exist with as many as 6 stages.

The 4 stages are sometimes known as the "Tennis" staging of hypovolemic shock, as the stages of blood loss (under 15% of volume, 15–30% of volume, 30–40% of volume and above 40% of volume) mimic the scores in a game of tennis: 15, 15–30, 30–40 and 40. It is basically the same as used in classifying bleeding by blood loss.

The signs and symptoms of the major stages of hypovolemic shock include:

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.

Electric shock is also used as a medical therapy, under carefully controlled conditions:

- Electroconvulsive therapy or ECT is a psychiatric therapy for mental illness. The objective of the therapy is to induce a seizure for therapeutic effect. There is no conscious sensation of the electric shock because of the anesthesia used beforehand. Convulsive therapy was introduced in 1934 by Hungarian neuropsychiatrist Ladislas J. Meduna who, believing mistakenly that schizophrenia and epilepsy were antagonistic disorders, induced seizures first with camphor and then metrazol (cardiazol). The first patient was treated by Lucio Bini and Ugo Cerlettiin. ECT is generally administered three times a week for about 8-12 treatments.

- As a surgical tool for cutting or coagulation. An "Electrosurgical Unit" (or ESU) uses high currents (e.g. 10 amperes) at high frequency (e.g. 500 kHz) with various schemes of amplitude modulation to achieve the desired result - cut or coagulate - or both. These devices are safe when used correctly.

- As a treatment for fibrillation or irregular heart rhythms: see defibrillator and cardioversion.

- As a method of pain relief: see Transcutaneous Electrical Nerve Stimulator (more commonly referred to as a TENS unit).

- As an aversive punishment for conditioning of developmentally delayed individuals with severe behavioral problems. This controversial skin-shock method is employed only at the Judge Rotenberg Educational Center, a special needs school in Massachusetts.

- As a treatment for Hyperhidrosis with the device called iontophoresis

- As part of electrodiagnosis diagnostic tests including nerve conduction studies and electromyography.

- For genetic engineering and gene delivery using a non-viral vector system electroporation

There were 550 reported electrocutions in the US in 1993, 2.1 deaths per million inhabitants. At that time, the incidence of electrocutions was decreasing. Electrocutions in the workplace make up the majority of these fatalities. From 1980–1992, an average of 411 workers were killed each year by electrocution. A recent study conducted by the National Coroners Information System (NCIS) in Australia has revealed three-hundred and twenty-one (321) closed case fatalities (and at least 39 case fatalities still under coronial investigation) that had been reported to Australian coroners where a person died from electrocution between July 2000 and October 2011.

In Sweden, Denmark, Finland and Norway the number of electric deaths per million inhabitants was 0.6, 0.3, 0.3 and 0.2, respectively, in years 2007-2011.

People who survive electrical trauma may suffer a host of injuries including loss of consciousness, seizures, aphasia, visual disturbances, headaches, tinnitus, paresis, and memory disturbances. Even without visible burns, electric shock survivors may be faced with long-term muscular pain and discomfort, fatigue, headache, problems with peripheral nerve conduction and sensation, inadequate balance and coordination, among other symptoms. Electrical injury can lead to problems with neurocognitive function, affecting speed of mental processing, attention, concentration, and memory. The high frequency of psychological problems is well established and may be multifactorial. As with any traumatic and life-threatening experience, electrical injury may result in post traumatic psychiatric disorders. There exist several non-profit research institutes that coordinate rehabilitation strategies for electrical injury survivors by connecting them with clinicians that specialize in diagnosis and treatment of various traumas that arise as a result of electrical injury.

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.

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.

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.

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.

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.

Initial diagnosis can be challenging, as there are a number of differential diagnoses, including tension pneumothorax, and acute heart failure. In a trauma patient presenting with PEA (pulseless electrical activity) in the absence of hypovolemia and tension pneumothorax, the most likely diagnosis is cardiac tamponade.

Signs of classical cardiac tamponade include three signs, known as Beck's triad. Low blood pressure occurs because of decreased stroke volume, jugular-venous distension due to impaired venous return to the heart, and muffled heart sounds due to fluid buildup inside the pericardium.

Other signs of tamponade include pulsus paradoxus (a drop of at least 10 mmHg in arterial blood pressure with inspiration), and ST segment changes on the electrocardiogram, which may also show low voltage QRS complexes, as well as general signs and symptoms of shock (such as fast heart rate, shortness of breath and decreasing level of consciousness). However, some of these signs may not be present in certain cases. A fast heart rate, although expected, may be absent in people with uremia and hypothyroidism.

In addition to the diagnostic complications afforded by the wide-ranging differential diagnosis for chest pain, diagnosis can be additionally complicated by the fact that patients will often be weak or faint at presentation. For instance, a fast rate of breathing and difficulty breathing on exertion that progresses to air hunger at rest can be a key diagnostic symptom, but it may not be possible to obtain such information from patients who are unconscious or who have convulsions at presentation.

Tamponade can often be diagnosed radiographically. Echocardiography, which is the diagnostic test of choice, often demonstrates an enlarged pericardium or collapsed ventricles. A large cardiac tamponade will show as an enlarged globular-shaped heart on chest x-ray. During inspiration, the negative pressure in the thoracic cavity will cause increased pressure into the right ventricle. This increased pressure in the right ventricle will cause the interventricular septum to bulge towards the left ventricle, leading to decreased filling of the left ventricle. At the same time, right ventricle volume is markedly diminished and sometimes it can collapse.

A radiographic evaluation using an X-ray, CT scan, or MRI can determine if there is damage to the spinal column and where it is located. X-rays are commonly available and can detect instability or misalignment of the spinal column, but do not give very detailed images and can miss injuries to the spinal cord or displacement of ligaments or disks that do not have accompanying spinal column damage. Thus when X-ray findings are normal but SCI is still suspected due to pain or SCI symptoms, CT or MRI scans are used. CT gives greater detail than X-rays, but exposes the patient to more radiation, and it still does not give images of the spinal cord or ligaments; MRI shows body structures in the greatest detail. Thus it is the standard for anyone who has neurological deficits found in SCI or is thought to have an unstable spinal column injury.

Neurological evaluations to help determine the degree of impairment are performed initially and repeatedly in the early stages of treatment; this determines the rate of improvement or deterioration and informs treatment and prognosis. The ASIA Impairment Scale outlined above is used to determine the level and severity of injury.

Early diagnosis is necessary to properly manage sepsis, as initiation of rapid therapy is key to reducing deaths from severe sepsis.

Within the first three hours of suspected sepsis, diagnostic studies should include white blood cell counts, measuring serum lactate, and obtaining appropriate cultures before starting antibiotics, so long as this does not delay their use by more than 45 minutes. To identify the causative organism(s), at least two sets of blood cultures using bottles with media for aerobic and anaerobic organisms should be obtained, with at least one drawn through the skin and one drawn through each vascular access device (such as an IV catheter) in place more than 48 hours. Bacteria are present in the blood in only about 30% of cases. Another possible method of detection is by polymerase chain reaction. If other sources of infection are suspected, cultures of these sources, such as urine, cerebrospinal fluid, wounds, or respiratory secretions, also should be obtained, as long as this does not delay the use of antibiotics.

Within six hours, if blood pressure remains low despite initial fluid resuscitation of 30 ml/kg, or if initial lactate is ≥ 4 mmol/l (36 mg/dl), central venous pressure and central venous oxygen saturation should be measured. Lactate should be re-measured if the initial lactate was elevated. Within twelve hours, it is essential to diagnose or exclude any source of infection that would require emergent source control, such as necrotizing soft tissue infection, infection causing inflammation of the abdominal cavity lining, infection of the bile duct, or intestinal infarction. A pierced internal organ (free air on abdominal x-ray or CT scan), an abnormal chest x-ray consistent with pneumonia (with focal opacification), or petechiae, purpura, or purpura fulminans may be evident of infection.

A 2013 review concluded moderate-quality evidence exists to support use of the procalcitonin level as a method to distinguish sepsis from non-infectious causes of SIRS. The same review found the sensitivity of the test to be 77% and the specificity to be 79%. The authors suggested that procalcitonin may serve as a helpful diagnostic marker for sepsis, but cautioned that its level alone cannot definitively make the diagnosis. A 2012 systematic review found that soluble urokinase-type plasminogen activator receptor (SuPAR) is a nonspecific marker of inflammation and does not accurately diagnose sepsis. This same review concluded, however, that SuPAR has prognostic value, as higher SuPAR levels are associated with an increased rate of death in those with sepsis.