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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 recent study by Salcido et al. (2010) ascertained rearrest in all initial and rearrest rhythms treated by any level of Emergency Medical Service (EMS), finding a rearrest rate of 36% and a lower but not significantly different rate of survival to hospital discharge in cases with rearrest compared to those without rearrest.
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.
The absence of a pulse confirms a clinical diagnosis of cardiac arrest, but PEA can only be distinguished from other causes of cardiac arrest with a device capable of electrocardiography (ECG/EKG). In PEA, there is organised or semi-organised electrical activity in the heart as opposed to asystole (flatline)or to the disorganised electrical activity of either ventricular fibrillation or ventricular tachycardia.
To determine the need for referral to a specialized burn unit, the American Burn Association devised a classification system. Under this system, burns can be classified as major, moderate and minor. This is assessed based on a number of factors, including total body surface area affected, the involvement of specific anatomical zones, the age of the person, and associated injuries. Minor burns can typically be managed at home, moderate burns are often managed in hospital, and major burns are managed by a burn center.
The size of a burn is measured as a percentage of total body surface area (TBSA) affected by partial thickness or full thickness burns. First-degree burns that are only red in color and are not blistering are not included in this estimation. Most burns (70%) involve less than 10% of the TBSA.
There are a number of methods to determine the TBSA, including the Wallace rule of nines, Lund and Browder chart, and estimations based on a person's palm size. The rule of nines is easy to remember but only accurate in people over 16 years of age. More accurate estimates can be made using Lund and Browder charts, which take into account the different proportions of body parts in adults and children. The size of a person's handprint (including the palm and fingers) is approximately 1% of their TBSA.
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."
A diagnosis of bradycardia in adults is based on a heart rate less than 60 BPM. This is determined usually either by palpation or electrocardiography.
If symptoms occur, a determination of electrolytes may be helpful in determining the underlying cause.
Commotio cordis may also occur in other situations, such as in children who are punished with blows over the precordium, cases of torture, and frontal collisions of motor vehicles (the impact of the steering wheel against the thorax, although this has decreased substantially with the use of safety belts and air bags). In one fatality, the impact to the chest was the result of an exploding whipping cream canister.
In contrast, the precordial thump (hard blows given over the precordium with a closed fist to revert cardiac arrest) is a sanctioned procedure for emergency resuscitation by trained health professionals witnessing a monitored arrest when no equipment is at hand, endorsed by the latest guidelines of the International Liaison Committee on Resuscitation. It has been discussed controversially, as—in particular in severe hypoxia—it may cause the opposite effect (i.e., a worsening of rhythm—commotio cordis). In a normal adult, the energy range involved in the precordial thump is five to 10 times below that associated with commotio cordis.
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.
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.
Electroanalgesia poses serious health problems in those patients who need other electrical equipment in their bodies, such as pacemakers and hearing aids, because the electrical signals of the multiple devices can interfere with each other and fail. People with heart problems, such as irregular heartbeat, are also at risk because the devices can throw off the normal electrical signal of the heart.
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.
The treatment of bradycardia is dependent on whether or not the person is stable or unstable. If oxygen saturations are low, supplemental oxygen should be provided.
Cardiac arrhythmia are often first detected by simple but nonspecific means: auscultation of the heartbeat with a stethoscope, or feeling for peripheral pulses. These cannot usually diagnose specific arrhythmia but can give a general indication of the heart rate and whether it is regular or irregular. Not all the electrical impulses of the heart produce audible or palpable beats; in many cardiac arrhythmias, the premature or abnormal beats do not produce an effective pumping action and are experienced as "skipped" beats.
The simplest "specific" diagnostic test for assessment of heart rhythm is the electrocardiogram (abbreviated ECG or EKG). A Holter monitor is an EKG recorded over a 24-hour period, to detect arrhythmias that may happen briefly and unpredictably throughout the day.
A more advanced study of the heart's electrical activity can be performed to assess the source of the aberrant heart beats. This can be accomplished in an electrophysiology study, an endovascular procedure that uses a catheter to "listen" to the electrical activity from within the heart, additionally if the source of the arrhythmias is found, often the abnormal cells can be ablated and the arrhythmia can be permanently corrected. "" (TAS) instead uses an electrode inserted through the esophagus to a part where the distance to the posterior wall of the left atrium is only approximately 5–6 mm (remaining constant in people of different age and weight). Transesophageal atrial stimulation can differentiate between atrial flutter, AV nodal reentrant tachycardia and orthodromic atrioventricular reentrant tachycardia. It can also evaluate the risk in people with Wolff–Parkinson–White syndrome, as well as terminate supraventricular tachycardia caused by re-entry.
Percutaneous electrical nerve stimulation, or PENS, is used mainly in the treatment of intractable pain associated with chronic low back pain syndrome, cancer, and other disorders. It is a technique involving insertion of an ultra-fine acupuncture needle which probes into the soft tissues or muscles to electrically stimulate nerve fibers in the sclerotomal, myotomal, or dermatomal distribution corresponding to the patient's pain symptoms. PENS is related to both electroacupuncture and transcutaneous electrical nerve stimulation.
The method of cardiac rhythm management depends firstly on whether or not the affected person is stable or unstable. Treatments may include physical maneuvers, medications, electricity conversion, or electro- or cryo-cautery.
In the United States, people admitted to the hospital with cardiac arrhythmia and conduction disorders with and without complications were admitted to the intensive care unit more than half the time in 2011.
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.
In general, the minimal evaluation of atrial fibrillation should be performed in all individuals with AF. The goal of this evaluation is to determine the general treatment regimen for the individual. If results of the general evaluation warrant it, further studies may then be performed.
Limited studies have suggested that screening for atrial fibrillation in those 65 years and older increases the number of cases of atrial fibrillation detected.
An electrocardiogram can be used to identify a ventricular escape beat. The QRS portion of the electrocardiogram represents the ventricular depolarisation; in normal circumstances the QRS complex forms a sharp sudden peak. For a patient with a ventricular escape beat, the shape of the QRS complex is broader as the impulse can not travel quickly via the normal electrical conduction system.
Ventricular escape beats differ from ventricular extrasystoles (or premature ventricular contractions), which are spontaneous electrical discharges of the ventricles. These are not preceded by a pause; on the contrary they are often followed by a compensatory pause.
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.
Third degree AV block can be treated with Cilostazol which acts to increase Ventricular escape rate
Myofibre break-up, abbreviated MFB, is associated with ventricular fibrillation leading to death. Histomorphologically, MFB is characterized by fractures of the cardiac myofibres perpendicular to their long axis, with squaring of the myofibre nuclei.