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.

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

Similar to cardiac arrest, rearrest is treated with both cardiopulmonary resuscitation and defibrillation. The goal of treatment is to reestablish a self perfusing heart through correction of the electrical activity within the heart. CPR entails chest compressions along with rescue breaths, while defibrillation involves a biphasic shock across the chest with the purpose of restarting the electrical activity of the heart.

Anti-arrythmic drugs are commonly given during the ROSC phase. These drugs may include lidocaine and amiodarone.

Current research seeks to predict the event of rearrest after patients have already achieved ROSC. Biosignals, such as electrocardiogram (ECG), have the potential to predict the onset of rearrest and are currently being investigated to preemptively warn health care providers that rearrest could be imminent.

A stronger pulse detector would also contribute to lowering the rate of rearrest. If the resuscitator could accurately know when the patient has achieved ROSC, there would be less instances of chest compressions being provided when a native pulse is present.

Most cases are fatal. Automated external defibrillators have helped increase the survival rate to 35%. Defibrillation must be started as soon as possible (within 3 minutes) for maximal benefit. Commotio cordis is the leading cause of fatalities in youth baseball in the US, with two to three deaths per year. It has been recommended that "communities and school districts reexamine the need for accessible automatic defibrillators and cardiopulmonary resuscitation-trained coaches at organized sporting events for children."

Commotio cordis is a very rare event, but nonetheless is often considered when an athlete presents with sudden cardiac death. Some of the sports which have a risk for this cause of trauma are baseball, American football, association football, ice hockey, polo, rugby football, cricket, softball, pelota, fencing, lacrosse, boxing, karate, kung fu, and other martial arts. Children are especially vulnerable, possibly due to the mechanical properties of their thoracic skeleton. From 1996 to spring 2007, the USA National Commotio Cordis Registry had 188 cases recorded, with about half occurring during organized sports. Almost all (96%) of the victims were male, the mean age of the victims during that period was 14.7 years, and fewer than one in five survived the incident.

Cardiac resuscitation guidelines (ACLS/BCLS) advise that Cardiopulmonary resuscitation should be initiated promptly to maintain cardiac output until the PEA can be corrected. The approach in treatment of PEA is to treat the underlying cause, if known (e.g. relieving a tension pneumothorax). Where an underlying cause for PEA cannot be determined and/or reversed, the treatment of pulseless electrical activity is similar to that for asystole. There is no evidence that external cardiac compression can increase cardiac output in any of the many scenarios of PEA, such as hemorrhage, in which impairment of cardiac filling is the underlying mechanism producing loss of a detectable pulse.

An intravenous or intraosseous line should be started to provide medications through. The mainstay of drug therapy for PEA is epinephrine (adrenaline) 1 mg every 3–5 minutes. Although previously the use of atropine was recommended in the treatment of PEA/asystole, this recommendation was withdrawn in 2010 by the American Heart Association due to lack of evidence for therapeutic benefit. Epinephrine too has a limited evidence base, and it is recommended on the basis of its mechanism of action.

Sodium bicarbonate 1meq per kilogram may be considered in this rhythm as well, although there is little evidence to support this practice. Its routine use is not recommended for patients in this context, except in special situations (e.g. preexisting metabolic acidosis, hyperkalemia, tricyclic antidepressant overdose).

All of these drugs should be administered along with appropriate CPR techniques. Defibrillators cannot be used to correct this rhythm, as the problem lies in the response of the myocardial tissue to electrical impulses.

A theoretical explanation for the mechanism of pain reduction by transcranial electrostimulation, or TCES, suggests that the electrical stimulation activates the anti-nociceptive system in the brain, resulting in β-endorphin, serotonin and noradrenaline release. TCES can be used on people with cervical pain, chronic lower back syndrome, or migraines. It cannot be used on people with orthopedic or radiological potentially serious spinal conditions, hydrocephalus, epilepsy, glaucoma, malignant hypertension, pacemaker or other implanted electronic device; recent cerebral trauma, nervous system infection, skin lesions at sites of electrode placement; oncological disease; patients undergoing any other treatments for pain; any invasive therapy, e.g. surgery, within the last month. The equipment used is Pulse Mazor Instruments' Pulsatilla 1000, which consists of a headset with three electrodes, two that go behind the ears and one that goes on the forehead, that release set frequencies of electricity at set intervals.

The first cases of electroanalgesia were documented by Greek scholars, Plutarch and Socrates, who noticed numbing effects of standing in pools of water on a beach that contained electric fish. The Chinese practice of acupuncture, dating back to 3000 BCE, also utilizes the properties of electroanalgesia by stimulating specific nerves to produce electrical signals which produce pleasurable responses in the brain. Another ancient analgesic method, aging back to 5000 BCE in Sumer, is to use natural minerals, vitamins, and herbs, usually in a mixture with other natural products. Technology invented specifically for electroanalgesia emerged at the beginning of the 1900s.

Asystole (1860, from Modern Latin, from Greek privative a "not, without" + "systolē" "contraction") is the absence of ventricular contractions lasting longer than the maximum time sustainable for life, which is about 2 seconds for human life. Asystole is the most serious form of cardiac arrest and is usually irreversible. A cardiac flatline is the state of total cessation of electrical activity from the heart, which means no tissue contraction from the heart muscle and therefore no blood flow to the rest of the body.

Asystole should not be confused with very brief pauses in the heart's electrical activity, even those that produce a temporary flat line, in electrical activity that can occur in certain less severe abnormal rhythms. Asystole is different from very fine occurrences of ventricular fibrillation, though both have a poor prognosis, and untreated fine VF will lead to asystole. Faulty wiring, disconnection of electrodes and leads, and power disruptions should be ruled out.

Asystolic patients (as opposed to those with a "shockable rhythm" such as ventricular fibrillation or ventricular tachycardia, which can be potentially treated with defibrillation) usually present with a very poor prognosis: asystole is found initially in only about 28% of cardiac arrest cases, but only 15% of these patients ever leave the hospital alive, even with the benefit of an intensive care unit, with the rate being lower (only 6%) for those already prescribed drugs for high blood pressure.

Asystole is treated by cardiopulmonary resuscitation (CPR) combined with an intravenous vasopressor such as epinephrine (a.k.a. adrenaline). Sometimes an underlying reversible cause can be detected and treated (the so-called 'Hs and Ts', an example of which is hypokalaemia). Several interventions previously recommended—such as defibrillation (known to be ineffective on asystole, but previously performed in case the rhythm was actually very fine ventricular fibrillation) and intravenous atropine—are no longer part of the routine protocols recommended by most major international bodies. Asystole may be treated with 1 mg epinephrine by IV every 3–5 minutes as needed. Vasopressin 40 units by IV every 3–5 minutes may be used in place of the first and/or second doses of epinephrine, but doing so does not enhance outcomes.

Survival rates in a cardiac arrest patient with asystole are much lower than a patient with a rhythm amenable to defibrillation; asystole is itself not a "shockable" rhythm. Out-of-hospital survival rates (even with emergency intervention) are less than 2 percent.

Acute management is as for SVT in general. The aim is to interrupt the circuit. In the shocked patient, DC cardioversion may be necessary. In the absence of shock, inhibition at the AV node is attempted. This is achieved first by a trial of specific physical maneuvers such as holding a breath in or bearing down. If these maneuvers fail, using intravenous adenosine; causes complete electrical blockade at the AV node and interrupts the reentrant electrical circuit. Long-term management includes beta blocker therapy and radiofrequency ablation of the accessory pathway.

Treatment depends on the origin of the automatic tachycardia, however the mainstay of treatment is either antidysrhythmic medication or cardiac pacing. Specifically overdrive pacing may be used for all forms of automatic tachycardia; a pacemaker assumes control of the heart rhythm in overdrive pacing. In some cases ablation of the ectopic focus may be necessary.

Burns can be very painful and a number of different options may be used for pain management. These include simple analgesics (such as ibuprofen and acetaminophen) and opioids such as morphine. Benzodiazepines may be used in addition to analgesics to help with anxiety. During the healing process, antihistamines, massage, or transcutaneous nerve stimulation may be used to aid with itching. Antihistamines, however, are only effective for this purpose in 20% of people. There is tentative evidence supporting the use of gabapentin and its use may be reasonable in those who do not improve with antihistamines. Intravenous lidocaine requires more study before it can be recommended for pain.

Intravenous antibiotics are recommended before surgery for those with extensive burns (>60% TBSA). , guidelines do not recommend their general use due to concerns regarding antibiotic resistance and the increased risk of fungal infections. Tentative evidence, however, shows that they may improve survival rates in those with large and severe burns. Erythropoietin has not been found effective to prevent or treat anemia in burn cases. In burns caused by hydrofluoric acid, calcium gluconate is a specific antidote and may be used intravenously and/or topically. Recombinant human growth hormone (rhGH) in those with burns that involve more than 40% of their body appears to speed healing without affecting the risk of death.

Honey has been used since ancient times to aid wound healing and may be beneficial in first- and second-degree burns. There is tentative evidence that honey helps heal partial thickness burns. The evidence for aloe vera is of poor quality. While it might be beneficial in reducing pain, and a review from 2007 found tentative evidence of improved healing times, a subsequent review from 2012 did not find improved healing over silver sulfadiazine. There were only three randomized controlled trials for the use of plants for burns, two for aloe vera and one for oatmeal.

There is little evidence that vitamin E helps with keloids or scarring. Butter is not recommended. In low income countries, burns are treated up to one-third of the time with traditional medicine, which may include applications of eggs, mud, leaves or cow dung. Surgical management is limited in some cases due to insufficient financial resources and availability. There are a number of other methods that may be used in addition to medications to reduce procedural pain and anxiety including: virtual reality therapy, hypnosis, and behavioral approaches such as distraction techniques.

Pulseless electrical activity (PEA), also known as electromechanical dissociation, refers to cardiac arrest in which the electrocardiogram shows a heart rhythm that should produce a pulse, but does not. Pulseless electrical activity is found initially in about 55% of people in cardiac arrest.

Under normal circumstances, electrical activation of muscle cells precedes mechanical contraction of the heart (known as "electromechanical coupling"). In PEA, there is electrical activity, but the heart either does not contract or there are other reasons this results in an insufficient cardiac output to generate a pulse and supply blood to the organs. While PEA is classified as a form of cardiac arrest, significant cardiac output may still be present which may be determined and best visualized by bedside ultrasound.

Cardiopulmonary resuscitation (CPR) is the first treatment for PEA, while potential underlying causes are identified and treated. The medication epinephrine may be administered. Survival is about 20%.

Emergency treatment is not needed if the person is asymptomatic or minimally symptomatic.

If a person is unstable, the initial recommended treatment is intravenous atropine. Doses less than 0.5 mg should not be used, as this may further decrease the rate. If this is not effective, intravenous inotrope infusion (dopamine, epinephrine) or transcutaneous pacing should be used. Transvenous pacing may be required if the cause of the bradycardia is not rapidly reversible.

In children, giving oxygen, supporting their breathing, and chest compressions are recommended.

Possible underlying causes, which may be treatable and reversible in certain cases, include the Hs and Ts.

- Hypovolemia

- Hypoxia

- Hydrogen ions (acidosis)

- Hypothermia

- Hyperkalemia or Hypokalemia

- Hypoglycemia

- Tablets or Toxins (drug overdose)

- Electric shock

- Tachycardia

- Cardiac Tamponade

- Tension pneumothorax

- Thrombosis (myocardial infarction or pulmonary embolism)

- Trauma (hypovolemia from blood loss)

While the heart is asystolic, there is no blood flow to the brain unless CPR or internal cardiac massage (when the chest is opened and the heart is manually compressed) is performed, and even then it is a small amount. After many emergency treatments have been applied but the heart is still unresponsive, it is time to consider pronouncing the patient dead. Even in the rare case that a rhythm reappears, if asystole has persisted for fifteen minutes or more, the brain will have been deprived of oxygen long enough to cause brain death.

There are many classes of antiarrhythmic medications, with different mechanisms of action and many different individual drugs within these classes. Although the goal of drug therapy is to prevent arrhythmia, nearly every anti arrhythmic drug has the potential to act as a pro-arrhythmic, and so must be carefully selected and used under medical supervision.

A number of other drugs can be useful in cardiac arrhythmias.

Several groups of drugs slow conduction through the heart, without actually preventing an arrhythmia. These drugs can be used to "rate control" a fast rhythm and make it physically tolerable for the patient.

Some arrhythmias promote blood clotting within the heart, and increase risk of embolus and stroke. Anticoagulant medications such as warfarin and heparins, and anti-platelet drugs such as aspirin can reduce the risk of clotting.

Sudden cardiac arrest is the leading cause of death in the industrialised world. It exacts a significant mortality with approximately 70,000 to 90,000 sudden cardiac deaths each year in the United Kingdom, and survival rates are only 2%. The majority of these deaths are due to ventricular fibrillation secondary to myocardial infarction, or "heart attack". During ventricular fibrillation, cardiac output drops to zero, and, unless remedied promptly, death usually ensues within minutes.

People with atrial fibrillation and rapid ventricular response are often treated with amiodarone or procainamide to stabilize their heart rate. Procainamide and cardioversion are now accepted treatments for conversion of tachycardia found with WPW. Amiodarone was previously thought to be safe in atrial fibrillation with WPW, but after several cases of ventricular fibrillation, it is no longer recommended in this clinical scenario.

AV node blockers should be avoided in atrial fibrillation and atrial flutter with WPW or history of it; this includes adenosine, diltiazem, verapamil, other calcium channel blockers, and beta blockers. They can exacerbate the syndrome by blocking the heart's normal electrical pathway (therefore favoring 1:1 atrial to ventricle conduction through the pre-excitation pathway, potentially leading to unstable ventricular arrhythmias).

Ouabain infusion decreases ventricular escape time and increases ventricular escape rhythm. However, a high dose of ouabain can lead to ventricular tachycardia.

The definitive treatment of WPW is the destruction of the abnormal electrical pathway by radiofrequency catheter ablation. This procedure is performed by cardiac electrophysiologists. Radiofrequency catheter ablation is not performed in all individuals with WPW because inherent risks are involved in the procedure. When performed by an experienced electrophysiologist, radiofrequency ablation has a high success rate. Findings from 1994 indicate success rates of as high as 95% in people treated with radiofrequency catheter ablation for WPW. If radiofrequency catheter ablation is successfully performed, the condition is generally considered cured. Recurrence rates are typically less than 5% after a successful ablation. The one caveat is that individuals with underlying Ebstein's anomaly may develop additional accessory pathways during progression of their disease.

Defibrillation is the definitive treatment of ventricular fibrillation, whereby an electrical current is applied to the ventricular mass either directly or externally through pads or paddles, with the aim of depolarising enough of the myocardium for co-ordinated contractions to occur again. The use of this is often dictated around the world by Advanced Cardiac Life Support or Advanced Life Support algorithms, which is taught to medical practitioners including doctors, nurses and paramedics and also advocates the use of drugs, predominantly epinephrine, after every second unsuccessful attempt at defibrillation, as well as cardiopulmonary resuscitation (CPR) in between defibrillation attempts. Though ALS/ACLS algorithms encourage the use of drugs, they state first and foremost that defibrillation should not be delayed for any other intervention and that adequate cardiopulmonary resuscitation be delivered with minimal interruption.

The precordial thump is a manoeuver promoted as a mechanical alternative to defibrillation. Some advanced life support algorithms advocate its use once and only in the case of witnessed and monitored V-fib arrests as the likelihood of it successfully cardioverting a patient are small and this diminishes quickly in the first minute of onset.

Patients who survive a 'V-fib arrest' and who make a good recovery from this are often considered for implantation of an implantable cardioverter-defibrillator, which can quickly deliver this same life-saving defibrillation should another episode of ventricular fibrillation occur outside a hospital environment.