Table of contents :

• galvanic or direct currents (D.C.) : unidirectional electric current derived from a chemical battery => galvanotherapy / galvanization : the therapeutic use of galvanic current.
• inductothermy : the production of artificial fever by electric induction
• electrolithotrity : the disintegration of calculi by the application of electric current
• defibrillation : termination of atrial fibrillation (AF), sustained ventricular tachycardia or ventricular fibrillation (VF) at 5 seconds post-electroshock

Epidemiology : Kouwenhouven showed that electrical shocks applied to dogs within 30 seconds of an induced ventricular fibrillation (VF) could produce a 98% rate of resuscitation; however, those shocked after 2 minutes of VF had only a 27% resuscitation rate. This gave rise to the goal of early defibrillation for VF and ventricular tachycardia (VT). Up to 300 V (continue current) are administered for some ms either directly or through electrodes placed on the chest wall. Paddles are placed over the chest along the heart axis.
• cardioversion : the restoration of normal rhythm of the heart by electrical shock
• cardioverter : an energy-storage capacitor-discharge type of condenser which is discharged with an inductance; it delivers a direct-current shock which restores normal rhythm of the heart.
• automatic implantable cardioverter-defibrillator (AICD) : in 1980, Dr. Michel Mirowski revolutionized the management of ventricular arrhythmias when he demonstrated the efficacy of the automatic implantable defibrillator^ref. With the implantable cardioverter-defibrillator (ICD), once sustained VT or VF is detected, an electrical current is directed across a large portion of the myocardium to depolarize most of the ventricular tissue, thereby allowing an organized rhythm to return. Despite initial criticism and considerable controversy^ref, the ICD has gained widespread acceptance and implementation, with an estimated 55,000 such devices now implanted in the United States annually. This dramatic acceleration in implantation is a direct reflection of the rapidly expanding list of approved indications for ICD therapy in recent years^ref. Indications for implantable cardioverter-defibrillator therapy :
• class I (general agreement that it is beneficial, useful, and effective):
• 1. cardiac arrest due to VF or VT not due to a transient or reversible cause.
• 2. spontaneous sustained VT in association with structural heart disease.
• 3. syncope of undetermined origin with clinically relevant, hemodynamically significant, sustained VT or VF induced at electrophysiologic study when drug therapy is ineffective, not tolerated, or not preferred.
• 4. nonsustained VT in patients with coronary disease, prior MI, LV dysfunction, and inducible VF or sustained VT at electrophysiologic study that is not suppressible by a Class I antiarrhythmic drug.
• 5. spontaneous sustained VT in patients without structural heart disease not amenable to other treatments.
• class IIa (weight of opinion is in favor of usefulness/efficacy):
• Patients with left ventricular ejection fraction of ? 30% at least 1 month after MI and 3 months after coronary artery revascularization.
• class IIb (usefulness/efficacy is less well established by evidence/opinion):
• 6. cardiac arrest presumed to be due to VF when electrophysiologic testing is precluded by other medical conditions.
• 7. severe symptoms (e.g., syncope) attributable to ventricular tachyarrhythmias in patients awaiting cardiac transplantation.
• 8. familial or inherited conditions with a high risk for life-threatening ventricular tachyarrhythmias such as long QT syndrome or hypertrophic cardiomyopathy.
• 9. nonsustained VT with coronary artery disease, prior MI, and LV dysfunction, and inducible sustained VT or VF at electrophysiologic study.
• 10. recurrent syncope of undetermined origin in the presence of ventricular dysfunction and inducible ventricular arrhythmias at electrophysiologic study when other causes of syncope have been excluded.
• 11. syncope of unexplained origin or family history of unexplained sudden cardiac death in association with typical or atypical right bundle-branch block and ST-segment elevation (Brugada syndrome).
• class 3 (evidence/agreement that procedure is not indicated or is harmful)
• syncope of undetermined cause in a patient without inducible ventricular tachyarrhythmias and without structural heart disease)
• incessant VT or VF
• VF or VT resulting from arrhythmias amenable to surgical or catheter ablation; e.g. atrial arrhythmias associated with the Wolff-Parkinson-White syndrome, right ventricular outflow tract VT, idiopathic LV tachycardia, or fascicular VT
• ventricular tachyarrhythmias due to a transient or reversible disorder when correction of the disorder is considered feasible and likely to substantially reduce the risk of recurrent arrhythmia
Patients with severe heart failure in New York Heart Association (NYHA) functional class III–IV, low left ventricular ejection fraction, and broad QRS have been shown to benefit from biventricular pacing in randomised crossover and parallel trials^{ref1, ref2, ref3, ref4, ref5} concerning symptomatic improvement such as exercise tolerance and quality of life
• clinical effects of biventricular pacing
• improves:
• quality of life
• exercise tolerance
• NYHA class
• LV ejection fraction
• LV dimensions
• heart rate variability
• reduces:
• total and heart failure related hospitalisations
• heart rate
• indications for biventricular pacing
• severe NYHA class III–IV heart failure despite optimal drug treatment
• aetiology non-ischaemic or ischaemic heart disease
• QRS >130 ms
• LVEDD >55 mm
• LVEF <35%
The results are less clear for those with mild heart failure where further studies are needed. However, the evidence at large is based on sample size calculations made for six month follow up^{ref1, ref2, ref3, ref4, ref5}. Therefore it remains unknown whether the effects on biventricular pacing are long lasting in terms of years and whether morbidity and mortality is influenced. Although observational and controlled studies have demonstrated a reduced need for heart failure related hospitalisations during biventricular pacing^{ref1, ref2, ref3, ref4, ref5, ref6}, no study as yet with mortality as the primary outcome has been published. Therefore, whether cardiac resynchronisation therapy influences survival remains to be demonstrated in the recently concluded COMPANION and the ongoing CARE-HF study. These both have hospitalisations and mortality as the primary outcome^{ref1, ref2}. The MUSTIC trial was not designed as a mortality study^{ref1, ref2, ref3}. Nevertheless, the two year survival rate in 104 patients on biventricular pacing was reported to be 80%. The annual mortality rate was 10%, which is lower than could be expected in these former NYHA class III patients. The causes of death were sudden (40%) and heart failure death (40%), and other causes (20%). There is thus no direct evidence to date that the risk for sudden cardiac death is reduced by biventricular pacing. Recently the use of prophylactic implantable cardioverter-defibrillators (ICD) has been suggested in patients with coronary artery disease and reduced left ventricular ejection fraction^{ref1, ref2}. In one study the benefit of a prophylactic defibrillator was greater in those with broad QRS^ref. Therefore, it could be speculated that a prophylactic defibrillator should be added to a biventricular pacemaker in the treatment of the severe heart failure patient with intraventricular conduction disturbance. The aim of this paper is to discuss the evidence for this. There is little to suggest that biventricular pacing can affect arrhythmia incidence. It could, however, be speculated that since biventricular pacing reduces the risk for bradycardia, the risk for bradyarrhythmia related sudden death—which accounts for a substantial proportion of sudden cardiac death in severe heart failure—would be reduced by pacing^{ref1, ref2}. ß Blocker treatment reduces sudden cardiac death by 40%, suggesting that ß blockers reduce the risk for ventricular tachycardia^{ref1, ref2}. Therefore, the introduction of a biventricular pacemaker could reduce the risk for sudden cardiac death both by preventing bradycardia and by enabling the introduction or up-titration of ß blocker treatment to optimal dose. From the MUSTIC and the PATH-CHF studies, 2 RCTs, we know that heart rate is reduced and heart rate variability improved by long term biventricular pacing^ref. However, whether biventricular pacing per se prevents ventricular tachyarrhythmia remains doubtful. Only one small study indicates that the number of ventricular extra-beats, salvos, and duration of ventricular tachycardia were reduced during biventricular compared control pacing^ref. However, interesting data have emerged from studies in which the primary indication for device implantation was an indication for defibrillator treatment. CONTAK-CD was a randomised crossover study of 490 patients with a classical indication for defibrillator treatment in combination with NYHA functional class II–IV heart failure and low ejection fraction. The first part of this study was a crossover comparison between three months each of ICD and biventricular pacing to ICD treatment alone concerning symptomatic improvement and safety. Of 581 patients included in the study, 490 were implanted: 245 were randomised to the combined treatment and the other 245 to ICD treatment alone. In contrast to biventricular pacing studies, somewhat more patients (66%) had ischaemic heart disease as the underlying aetiology, and patients with NYHA class II were also included.18 The utilisation of antitachycardia pacing occurred in 9.4% of the patients in both groups. Shock treatment was administered in 19.2% of the 245 patients randomised to ICD and biventricular pacing treatment compared to 18% of those 245 subjects assigned to ICD treatment alone. Thus, biventricular pacing neither promoted nor reduced the delivery of ICD treatment in these patients. The value of prophylactic ICD treatment in ischaemic and dilated cardiomyopathy has recently been studied^{ref1, ref2, ref3}. The MADIT II trial included patients with prior myocardial infarction and low ejection fraction. No arrhythmia screening, either non-invasive or invasive, was required. Importantly, less than a third of patients had NYHA class III heart failure and patients in class IV were excluded from the study. Of the 1232 patients, 742 were randomly assigned to receive a prophylactic ICD and 490 were assigned to the control group. Overall a 31% reduction in the risk of death at any interval during the four year follow up among patients in the defibrillator group compared to the conventional treatment group was found. However, the benefit in terms of number of saved deaths by ICD was relatively small: 106 deaths (14.2%) in the ICD arm compared to 97 deaths (19.8%) in the conventional arm, corresponding to an absolute reduction of mortality of 5.6%. Moreover, the survival benefit by ICD treatment became apparent only after nine months. Interestingly, hazard ratios in this study indicated that the greater the QRS width, the greater the survival benefit in the ICD arm. This was further examined by Zareba who looked for non-invasive ECG criteria to identify patients who derive the most benefit from ICD treatment (oral communication, NASPE 2002). There were only two independent risk factors for prognosis: atrial fibrillation and QRS width. The 3 year mortality in 530 patients with QRS width of just 120 ms was 37% in the control group compared to 24% in the ICD group—a 49% reduction in mortality resulting from ICD treatment. In those 364 patients with a QRS above 120 ms the three year mortality was 53% in the control group compared to 21% in the ICD group, translating to a mortality reduction of 63%. Thus, the reduction in mortality by ICD treatment was substantially greater in those with a wide QRS than in the MADIT-II population as a whole. Moreover, except for QRS width, there was no indication that non-invasive arrhythmia screening such as heart rate variability was of any value in mortality risk prediction. Therefore, it seems clear that a prophylactic ICD in combination with biventricular pacing is indicated in patients fulfilling the entry criteria for both the MADIT II and for biventricular pacing. In contrast, the beneficial value of prophylactic ICD treatment for patients with dilated cardiomyopathy remains unknown. Only one study so far aimed at studying exclusively such patients^ref. The CAT trial was a primary prevention study in 104 dilated cardiomyopathy patients followed for a mean of 5.5 years^ref. The study compared the survival benefit of ICD treatment to control treatment in patients with recent onset dilated cardiomyopathy, ejection fraction below 30%, and NYHA class II–III heart failure. Patients with NYHA class IV or symptomatic brady- or tachycardia were excluded. The primary end point in the study was one year total mortality. The study was terminated early because the all cause mortality at one year did not reach the expected 30% but was only 5.6%. The mean follow up time was 22 months. Drug treatment at baseline comprised angiotensin converting enzyme inhibitors in 96% of the subjects and ß blockers in only 4%. No report of amiodarone treatment is given. Survival rates of the 50 patients assigned to ICD treatment and those 54 patients assigned to the control group did not differ significantly between groups. In those assigned to ICD treatment the survival rate in those who experienced ventricular tachycardia during follow up was in fact worse than in those who did not. This indicates that activity in electrical disease paralleled overall infirmity. Moreover, the presence of non-sustained ventricular tachycardia on Holter ECG did not impact survival in the control group. In conclusion, the findings from this study do not indicate a survival benefit with prophylactic ICD treatment in patients with dilated cardiomyopathy and reduced left ventricular function (< 35%). It is not self evident that the evidence from these prophylactic ICD trials for primary prevention of sudden death can be applied automatically to severe heart failure patients eligible for biventricular pacing. In MADIT-II only 30% of patients had NYHA class III–IV heart failure and 50% had a QRS duration > 120 ms, with no information as to which proportion of these patients had both abnormalities. Thus, maximally 30–50% of them would have had a classical indication for biventricular pacing. Since at least 50% of patients in published studies on biventricular pacing had dilated cardiomyopathy as the underlying disorder, the evidence for the usefulness of a prophylactic ICD in biventricular pacing candidates is clearly called for^{ref1, ref2, ref3, ref4, ref5}. Moreover, Duncan and colleagues recently reported that patients with underlying dilated cardiomyopathy benefit more from biventricular pacing regarding symptom reduction and reverse left ventricular remodelling than those with underlying ischaemic heart disease^ref. In the CAT study, 35% of patients would have been candidates for biventricular pacing based on the functional class criteria, and 36% had left bundle branch block. Therefore, the question of whether a biventricular pacemaker should always be combined with a defibrillator should be answered by studies in which the main indication for device implantation was cardiac resynchronisation treatment. So far, only the COMPANION trial has included an ICD arm^ref. In the COMPANION study 2200 severe heart failure patients with a QRS duration above 120 ms were enrolled and randomised to receive optimal medical treatment alone, optimal medical treatment and biventricular pacing, or optimal medical treatment and biventricular pacing combined with an ICD in a 1:2:2 fashion. The primary end point was combined—that is, total mortality and all cause hospitalisations. The study was conducted on the assumption that an estimated event rate in the control arm of 40% should be reduced by 25% in both device arms. This required 2200 patients to be enrolled and to be followed for 2 years. The study was terminated early when 1600 patients had been enrolled because the primary end point had been reached in both device arms. The primary end point was significantly reduced by 20% both in the biventricular pacing arm and the biventricular pacing plus ICD arm. The secondary end point of total mortality alone was significantly reduced by 42% in the biventricular pacing plus ICD arm only. These results will have to be confirmed, but if true they point in favour of combined therapy for biventricular pacing candidates. Moreover, the results from the CARE-HF study, which are expected to emerge in 2004, will answer the remaining question of whether biventricular pacing alone reduces mortality^ref. Although heart rate and sympathetic nerve activity is reduced by cardiac resynchronisation therapy, there is no evidence that biventricular pacing prevents or provokes ventricular arrhythmias. Prophylactic ICD treatment is indicated in prior myocardial infarction patients with broad QRS. No solid evidence for the usefulness of a prophylactic ICD in dilated cardiomyopathy patients exist to date. Whether all patients with a classical indication for biventricular pacing should also receive a prophylactic ICD thus remains to be determined in ongoing trials^{ref1, ref2}
• electroversion : the act of electrically terminating a cardiac dysrhythmia
• ordinary manual defibrillator
• automated external defibrillators (AEDs) : survival rates for individuals with VF treated by AEDs have been reported between 0% and 31%. Comparatively, the survival rates for performing basic cardiopulmonary resuscitation (CPR) alone are reported between 0% and 6%^ref. Theoretically, even more lives could be saved if targeted members of the general public could obtain early access to and have training in the use of AEDs and CPR. Unfortunately, only about 16% of cardiac arrests occur in a public place. In 1947, Beck et al performed the first successful human defibrillation using specially designed internal cardiac paddles. He used 2 110-volt, 1.5-amp AC current shocks to resuscitate a 14-year-old boy who had become pulseless during elective chest surgery. In 1956, Zoll et al performed the first successful human external defibrillation using a 15-amp AC current that produced 710 volts applied across the chest for 0.15 seconds. In 1961, Alexander, Kleiger, and Lown first described the use of AC current for terminating VT. Work by Lown et al in the early 1960s demonstrated the superiority and safety of DC over AC for defibrillation. Ambulance-transported Belfast physicians first performed successful prehospital defibrillation in 1966. Defibrillation by emergency medical technicians (EMTs) without the presence of physicians was first performed in Portland, Oregon, in 1969 and was reported in 1972. In the early 1970s, Dr Arch Diack, Dr W Stanley Welborn, and Robert Rullman developed several prototype AEDs that were tested in the Portland area. They later formed the Cardiac Resuscitator Corporation to market their device. Prehospital trials began in Brighton, England, in 1980 using the Heart Aid. The device weighed 28 pounds and used an oral/epigastric and a precordial electrode to record ECG tracings and deliver electrical shocks. It was also capable of transcutaneously pacing the heart. In 1982, the US Food and Drug Administration (FDA) gave approval for EMT-defibrillation (EMT-D) clinical trials. Early US investigations of manual EMT-D were carried out in Washington, Iowa, Minnesota, and Tennessee. Today, over 50,000 AEDs are in use. In January 1994, the FDA issued a safety alert regarding AEDs manufactured by Laerdal. Some potential component problems were cited and the problem units were replaced; no further malfunctions were reported. Court battles ensued, and sales of Laerdal and Physio-Control AEDs were halted temporarily. The vast majority of the failures reported then (and with subsequent Physio-Control units) were caused by inappropriate application, poor maintenance, or lack of continuing education regarding the AEDs.

Early models of AEDs required inserting an oral/epigastric electrode and placing a second electrode on the chest. AEDs today require the placement of pads at the right sternal border and at the cardiac apex, along the heart axis. These electrodes serve to monitor and to defibrillate. AEDs also can inform the user when lead contact is poor, when the machine is preparing to defibrillate, when to check for a pulse, when a nonshockable rhythm is present, or when motion is detected.
• fully automatic AEDs shock at preprogrammed levels once VF or VT is sensed. Electrodes are placed in position and the AED is turned on after confirming that the patient is in cardiac arrest. The only way to prevent firing once the machine is committed to discharge is by turning off the AED.
• semiautomatic models inform the user when VF or VT is sensed, then advise defibrillation. The operator must press a button to deliver the shock. The user has the option to discharge the unit whenever necessary, even if the AED is not advising so. With many of the models, the operator can override the AED.
Early AEDs were designed to respond primarily to a HR > 150 electrical complexes per minute and a QRS amplitude > 0.15 mm. Presently, the ECG rhythm is analyzed via a combination of several methods. In addition to rate and amplitude criteria, the QRS is analyzed as to its slope, morphology, power spectrum density, and time away from the isoelectric baseline for preset levels defined as abnormal. Checks are made in 2- to 4-second intervals. In general, if abnormal complexes are detected for more than double the frequency of any other QRS for 3 consecutive checks, the AED will be primed to deliver a shock. Fine VF presents the greatest detection challenge. A trade-off exists between setting the amplitude criterion low enough to detect fine fibrillation, yet high enough to avoid shocking asystole or artifact. The sensitivity of detecting VF by AEDs has been reported as 76-96%. Specificity (correctly identifying non-VF rhythms) is reported to be nearly 100%.
• monophasic damped sine (MDS) waveform defibrillation delivers a charge in only one direction
• biphasic truncated exponential (BTE) waveform defibrillation delivers a charge in one direction for half of the shock and in the electrically opposite direction for the second half.
Dog studies have shown less conduction block and fewer ST segment changes after biphasic shock delivery than after monophasic delivery. Human studies have shown monophasic delivery to be equivalent to biphasic shocks for electrophysiologic study (EPS)-induced and prehospital VF and VT. Also, studies have shown that a biphasic waveform of 115 J is equivalent to a monophasic wave of about 200 J. Because of the decreased energy needed, most internal cardioversion defibrillators now use biphasic waveforms. Most manufacturers are converting to biphasic AEDs, as the lower amount of energy used can result in both longer battery life and a shorter time to full charge. Studies with implantable defibrillators have shown a difference in outcome related to electrode polarity. The only prospective study with AEDs, which was performed by Weaver in 1993, showed no difference in survival related to polarity while using a monophasic unit.
Patients must be medically unstable or pulseless before AED is applied. They should be pulseless before assessing the rhythm. This becomes increasingly important as more laypersons are given the opportunity to use AEDs. To prevent accidental shocking, the unit should not be analyzing the rhythm while CPR is performed. Most new units have a motion or CPR detector. The AED should not be used if the patient is seizing, and should be used only with caution in a moving vehicle. If being used on a patient in transport, frequent stops for pulse and AED monitoring checks should be made. Most units are designed to warn when motion or poor contact is detected. As with manual defibrillation, the chest does not need to be shaved prior to electrode placement but, if wet, it should be dried off. Water spots or nicks in the skin result in areas of decreased resistance and could lead to local burns as well as uneven and ineffective defibrillation. Proper maintenance is important, yet < 8% of AED users maintain their AED or replace their batteries according to the manufacturer's recommendations. Repeated check electrode warnings when electrodes seem properly placed may be from fractured electrodes. Replace them and retry.
AED selection factors :
• population density : areas with a population density < 100 persons /mile² received little benefit from AEDs^ref24. A recently reported study from Washington identified 172 sites of higher incidence (of 71,000 sites). Similar local assessments may aid in efficient public AED location.
• response time: on average, response time should be < 4-6 minutes for the patient to benefit from the use of AEDs.
• tiers : tiered response systems should have compatible equipment. If an AED is to be used by a first responder, defibrillators or their electrode wiring system should be compatible with the transporting units that follow.
• monitor : if the unit also is used by paramedics for monitoring and not just by AED technicians for cardiac arrest, a monitor screen is needed. Printout capabilities are also desirable
• event recording : a paper recording of the event may be sufficient for medical control; however, the need for a full set of data should influence equipment choice, since the data need to be downloaded. Because most of the data downloaded by AED units are not interchangeable, a setting in which data from various agencies needs to be collected and combined must use similar AEDs that can communicate; if they do not have this capability, data must be collected by hand.
Marketed AEDs :
• Agilent Technologies / Laerdal Medical Corp Heartstream FR2. Height: 6.6 cm, Width: 22 cm, Depth: 22 cm, Weight: 2.1 kg. Biphasic, monitor screen, lithium battery, visual/audio low battery indicator, manual override
• Medtronic Physio-Control LIFEPAK 500. Height: 10.2 cm, Width: 26.7 cm, Depth: 29.5 cm, Weight: Monophasic 3.2 kg, biphasic 2.9 kg. Monophasic and biphasic models, lead acid or lithium battery, visual/audio low battery indicator, 20-minute internal memory
• MRL/Medical Research AEDefibrillator. Height: 20.3 cm, Width: 22.8 cm, Depth: 7.6 cm, Weight: 2 kg. Monophasic or biphasic models
• SurVivaLinkFirstSave. Height: 8.4 cm, Width 26.9 cm, Depth: 31.5 cm, Weight: 3.4 kg. Biphasic variable energy delivery based on patient's measured impedance, lithium battery, visual/audio low battery indicator, 20-minute internal memory
• Zoll M Series(biphasic) Height: 17.2 cm, Width: 26.2 cm, Depth: 20.8 cm, Weight: 5.2 kg. Monitor screen, paper printout, lead acid battery, 4 MB internal memory, manual override
• PhilipsHeartStart Home Automated External Defibrillator (AED)


In the Brescia Early Defibrillation Study (BEDS), diffuse implementation of AEDs fully operated by trained volunteers and laypersons within a broad and unselected environment proved safe and was associated with a significantly higher long-term survival of CA victims^ref.
• countershock : a high-intensity DC shock delivered to the heart to interrupt ventricular fibrillation (VF) and restore synchronous electrical activity
Web resources :
• National Center for Early Defibrillation (NCED)
• ionic medicine : treatment by electrochemical means, as by
• cataphoresis : the passage of charged particles toward the negative pole (cathode) in electrophoresis.
• ionophoresis / iontophoresis / ionotherapy / iontherapy  : the introduction by means of the electric current, of ions of soluble salts into the tissues of the body, often for therapeutic purposes; a form of electro-osmosis
• magnetotherapy
• bracelets with a standard neodymium magnet with field strength of 170 to 200 mTesla or a weak magnet intended to produce 21 to 30 mTesla provide pain relief from osteoarthritis of the hip and knee. The change in a standard osteoarthritis index was significantly different between the standard and dummy magnet groups. The average score dropped from 10.7 to 7.8 in the standard group, and from 10.9 to 9.3 in the dummy group. Differences between the standard and weak magnets were not statistically significant - possibly because the strength of the weak magnets was found to range unintentionally between 21 and 169 mTesla. About 33% of participants in the standard and dummy groups correctly guessed their group assignment, often because they could see the bracelet exerted a magnetic force or not. Reduction in the osteoarthritis index score with the standard magnet, as well as the difference between the standard-magnet and dummy-magnet groups, is similar to that found in trials of frontline osteoarthritis treatments, including non-steroidal topical creams, oral nonsteroidal drugs (including COX-2 inhibitors) and exercise therapy^ref.
• neuromodulation denotes controlled electrical stimulation of the
• central nervous system
• electronarcosis : a treatment for psychiatric disorders using passage of an electric current through the brain via scalp electrodes, conditions being such as to produce a tonic phase similar to that of electroconvulsive therapy but limited or absent convulsions; it is both less effective and more likely to cause side effects than is electroconvulsive therapy
• electrosleep / cerebral electrotherapy : the use of low-intensity electricity, below the threshold for inducing convulsions, in the treatment of insomnia, anxiety, or depression
• electroshock therapy (EST) / electroconvulsive therapy (ECT) / seismotherapy : a treatment for mental disorders, primarily major depression, in which seizure and loss of consciousness are induced by application of brief pulses of low-voltage alternating current (100-150 V for 0.1-1 s) to the brain via scalp electrodes; a muscle relaxant, generally succinylcholine, is used to prevent injury during the seizure, together with atropine and thiopental. Awakening usually occurs within 10-15' and may be followed by a temporary confusional state; transient memory impairment may be present for weeks to as much as a year after treatment. ECT produces a therapeutic response in a majority of cases of major depression and is considered the strongest remedy in the treatment of severe depression, especially depression with psychotic features, and in the elderly. A stronger involvement of the hippocampus following experimental seizures compared with effects in that region induced by TMS and VNS might explain the consistent findings of the superiority of ECT in the most severe cases of affective disorder
• deep brain stimulation (DBS) is a completely implanted technique for
• improving movement disorders, such as Parkinson's disease and dystonia, by very focal electrical stimulation of the brain, a technique that employs well-established hardware (electrode and pulse generator/battery). Bilateral subthalamic neurostimulator (Itrel II, Medtronic) is a nerve stimulator with a battery is implanted under the skin in the chest. Wires are then used to link this to electrodes in the brain. The technique involves holes for the wires being drilled in the skull under anaesthetic. However, the patients have to be fully awake as the probes are positioned in the brain, so doctors could tell when the tremors stop
• it may be of potential use in rare cases of treatment-resistant cases of affective disorder
Kinetra^® Dual-Channel Neurostimulator (source : Medtronic) is based on Soletra/Activa Therapy neurostimulators. The Kinetra accommodates 2 extensions/leads, and thus provides bilateral neurostimulation from a single neurostimulator. This technology has had positive outcome of a study for treatment of depression and is also currently being evaluated in a Medtronic-sponsored multi-center US clinical trial as a therapy for treatment resistant epilepsy. To date, > 25,000 patients worldwide have benefited from Activa therapy.

• magnetic fields pass through tissue unimpeded, providing more control over the site and extent of stimulation than can be achieved with ECT. This enhanced control represents a means of focusing the treatment on target cortical structures thought to be essential to antidepressant response and reducing spread to medial temporal (MT) regions implicated in the cognitive side effects of ECT.
• magnetic seizure therapy (MST) : seizure
• transcranial magnetic stimulation (TMS) is unique among the current brain stimulation techniques because it is relatively non-invasive and painless. TMS markedly differs from vagus nerve stimulation, deep brain stimulation and magnetic seizure therapy, all of which require either an implanted prosthesis or general anesthesia, or both. It reborn in its modern form in 1985. Modern-day magnetic stimulators charge up to 3,000 V and produce peak currents of up to 8,000 A. TMS can be applied as :
• single pulses of stimulation can depolarise neurons and evoke measurable effects
• pairs of stimuli separated by variable intervals to the same or different brain areas
• trains of repetitive stimuli at various frequencies (repetitive TMS (rTMS)) can modify excitability of the underlying cerebral cortex at the stimulated site and also at remote areas along functional anatomical connections, but inhibits it at low stimulation frequencies
TMS is used as :
• basic neuroscience research instrument
• combining TMS with functional brain imaging in cognitive brain research
• potential clinical diagnostic tool
• therapy for
• tinnitus
• aphasia
• several different neuropsychiatric conditions
• treatment-resistant depression (TRD)
• schizophrenia
• PTSD
• OCD
• ADHD
• to enhance performance
Web resources :
• TMS at BioMag
• TMS in psychiatry at Medical University of South Carolina
• a current of 0.002 A (a fraction of that needed to power a digital watch) applied for 20 minutes is enough to produce a significant improvement and apart from an itchy sensation around the scalp electrode, subjects in the trials reported no side-effects. The volunteers were asked to name as many words as possible beginning with a particular letter. Given around 90 seconds, most people get around 20 words. But when the current is administered, volunteers were able to name around 20% more words than controls, who had the electrodes attached but no current delivered. A smaller current of one thousandth of an amp had no effect. Neurons in the prefrontal cortex fire off signals more easily after the current has gone by. But magnetic fields can cause seizures and also require bulky equipment to generate them. Low electric currents will offer a safer and more portable alternative. After running further safety tests, the effect of the current will be tested on patients with frontal temporal dementia, a brain disease that causes speech problems. The idea of using electrical current to boost brain activity dates back to experiments on animals in the 1950s : the early work showed some potential, but fell from favour because of a perceived link to electroconvulsive therapy
• peripheral nervous system
• transcutaneous electrical nerve stimulation (TENS) / transcutaneous nerve stimulation (TNS) : electrical stimulation of nerves for relief of pain, either by electrodes attached to the skin or by an apparatus manually held against the skin. It is a battery-powered unit which sends electrical impulses on or near the painful site. This causes a tingling sensation that reduces pain. It is used to treat acute pain (childbirth, post-operative pain, fractures, tennis elbow, and muscular strains) and chronic pain (neck and back pain, headache, migraine, arthritis, post-herpetic neuralgia, sciatica and lumbago)

Side effects : skin irritation or redness. Usually this disappears quickly or can be prevented by using alternative gels or electrodes
• electrophrenic respiration (EPR) / diaphragmatic or phrenic pacing : artificial respiration induced by electric stimulation of the phrenic nerve to produce rhythmic contractions of the diaphragm, done to provide ventilatory support in patients with diaphragmatic paralysis
• vagus nerve stimulation (VNS) is similar to deep brain stimulation in being well-established (for the treatment of refractory epilepsy), completely implanted, and having hardware that can be considered standard at the present time. Vagus nerve stimulation differs from deep brain stimulation, however, in that afferent stimulation of the vagus nerve results in diffuse effects on many regions throughout the brain. Although use of deep brain stimulation for applications beyond movement disorders will no doubt involve placing the stimulating electrode(s) in regions other than the thalamus, subthalamus, or globus pallidus, the use of vagus nerve stimulation for applications beyond epilepsy (for example, treatment-resistant depression (TRD) (used with limited results) and eating disorders) is unlikely to require altering the hardware significantly (although stimulation protocols may differ)^{ref1, ref2, ref3}
• implantable gastric stimulation (IGS) system : a stomach implant that is almost identical to a heart pacemaker could soon offer overweight patients a chance to beat their obesity, US surgeons hope. The device, which is to be tested at 8 hospitals, delivers electric pulses to the stomach, giving patients a feeling of fullness without eating. Doctors are unsure whether it works by stimulating nerves, muscles or glands, and warn that it is not a licence to become a couch potato. In gastric pacing, electrical stimulation of the antrum of the stomach causes reverse peristalsis and delayed gastric emptying. A U.S. trial of this procedure revealed that up to 40% of excess weight could be lost 2 years after treatment without complications^ref. Similarly, direct pyloric stimulation reduces gastric emptying and food intake in an animal model^ref. However, it is not yet known how these interventions work. A limited study showed that gastric pacing was associated with a decrease in CCK, somatostatin, and GLP-1 levels^ref and a mechanistic role for stimulation of vagal afferents has also been propounded. There is some support for this idea in that direct vagal stimulation is known to lead to weight loss in animal models^ref.
• galvanic vestibular stimulation (GVS) : remote controlled humans might sound a bizarre and nightmarish prospect, but Japanese researchers hope to harness the trick for computer gaming. By remotely stimulating a person's vestibular system - the fluid-filled tubes in the inner ear that guide their sense of balance - with electrodes placed on the skin just below the ear, researchers at NTT's research laboratories in Kanagawa have found a way to turn humans into oversized radio controlled vehicles. GVS unbalances a person so that they automatically veer left or right in an attempt to rebalance themselves. The NTT team developed a headset and a control unit similar to that used with remote-controlled toy cars. Volunteers were given a chance to experience GVS and, to the amusement of other visitors, were seen careening around the show floor under demonstrators' control. Taro Maeda and colleagues at NTT believe the system could primarily be used to make computer games feel more realistic. In a driving game, for example, a player could feel gravity shift as their car hurtles through a tight bend. I do think this could find an application in computer gaming : you could definitely use it to give the illusion of motion when going through some virtual environment. It certainly has some potential in this area : however, some evidence suggests extended use of vestibular stimulation at high current can cause tissue damage. Regulatory bodies would not allow GVS to be used in an uncontrolled way. GVS may also find use as a medical therapy, helping patients who have an impaired sense of balance. There certainly remains an opportunity in the medical sphere. Collins also points out that a US patent already exists for using GVS as a virtual reality tool. The approach was pioneered in the late 1990s by a company called Virtual Motion.
• variable currents
• interferential therapy
• farad-therapy / faradization : the therapeutic use of an interrupted current (multiple discharges of 100-200 V lasting each 1 ms), derived from an induction coil; principally for the stimulation of muscles and nerves.
• nanopulses are high-power electrical bolts that deliver millions of volts in a few billionths of a second and make mammalian cells undergo apoptosis (by flipping molecules in the cell membrane from the inside to the outside), rather than blowing them up (by contrast, long electric shocks explode cells and liberate toxic molecules that cause inflammation and pain). Longer shocks blow a cell apart, but leave the cell membrane unaffected while mixing up its insides. The pulses can
• make blood platelets clump together in the first stages of clotting
• fry bacteria and sterilize contaminated water
• shrink mouse tumours by over 50%, and is working on catheters or non-invasive ways to deliver the shocks to the body
• electroporation
• electrochemotherapy
• electro-nucleic acid transfection
• neuropacemaker : an implant device that relieves pain due to nerve injury.
• artificial cardiac pacemaker : a device that uses electrical impulses to reproduce or regulate the rhythms of the heart. Battery-driven and connected to the heart by leads and electrodes, it may be temporary or permanent and is inserted transvenously, transcutaneously, epicardially, or via the esophagus or coronary artery. Most pacemakers are either triggered or inhibited to modify output by sensing the intracardiac potential of one or more cardiac chambers; they have some degree of programmability and may also have antitachycardia functions. A 5 letter North American Society of Pacing and Electrophysiology (NASPE)/British Pacing and Electrophysiology Group (BPEG) generic (NBG) pacemaker code is used to categorize pacemakers by their combinations of these features

 

position category	antibradyarrhythmia functions
	I : chamber(s) paced	II : chamber(s) sensed	III : response to sensing	IV : programmability, rate modulation	V : antitachyarrhythmia function(s)
	O = none  A = atrium  V = ventricle  D = dual (A + V)	O = none  A = atrium  V = ventricle  D = dual (A + V)	O = none  T = triggers pacing  I = inhibits pacing  D = dual (T + I)	O = none  P = simple programmable  M = multiprogrammable  C = communicating  R = rate modulation	O = none  P = pacing (antitachyarrhythmia)  S = shock  D = dual (P + S)
manufacturer's designation only	S = single (either A or V)	S = single (either A or V)

• antitachycardia pacemaker : an implanted pacemaker that terminates tachycardia by delivering one or more pacing stimuli; it may require arrhythmia detection and device activation by the patient or may detect arrhythmias and deliver stimuli automatically.
• atrial asynchronous (AOO) pacemaker : an artificial cardiac pacemaker that stimulates the atrium at a constant rate, without sensing atrial or ventricular activity; rarely used except to initiate or terminate some tachycardias
• atrial demand inhibited (ADI) pacemaker : an artificial cardiac pacemaker that delivers stimuli to the atrium at a fixed rate in the absence of sensed atrial activity; spontaneous cardiac activity causes inhibition of pacemaker output, termination of the current stimulation cycle, and initiation of a new cycle
• AAIR pacemaker : an atrial demand inhibited pacemaker that is responsive to the patient's respiratory rate and thus to exercise and metabolic needs.
• atrial demand triggered (AAT) pacemaker : an artificial cardiac pacemaker that delivers stimuli to the atrium at a fixed rate in the absence of sensed atrial activity; spontaneous cardiac activity triggers pacemaker output, which falls ineffectively in the myocardial refractory period and initiates a new pacemaker stimulation cycle
• atrial synchronous ventricular (VAT) pacemaker : a dual chamber cardiac pacemaker that senses atrial activity and delivers a ventricular stimulus after a preset interval; used in patients with impaired atrioventricular conduction but normal sinus node function
• atrial synchronous ventricular inhibited (VDD) pacemaker : a dual chamber cardiac pacemaker similar to an atrial synchronous ventricular pacemaker but able to sense ventricular as well as atrial activity
• atrioventricular (AV) sequential pacemaker : an artificial cardiac pacemaker used in patients with abnormal sinus node function and impaired AV conduction; it senses ventricular, and sometimes atrial, activity and in addition to stimulating the atrium also stimulates the ventricle after an appropriate delay. Committed versions invariably deliver the ventricular stimulus while noncommitted versions deliver it only in the absence of interim ventricular activity
• DDD pacemaker : an artificial cardiac pacemaker that can sense and pace both the atria and ventricles; it is capable of operating in both triggered and inhibited modes as necessary.
• fully automatic or universal pacemaker : a term sometimes used to describe a DDD pacemaker, emphasizing that because it can be programmed to operate in one of numerous possible pacemaker modes under specific circumstances, it can be made to most closely approximate normal electrophysiologic functioning under a variety of conditions.
• DDDR pacemaker : a universal pacemaker that is responsive to the patient's respiratory rate and thus to exercise and metabolic needs.
• DDI pacemaker : a type of atrioventricular sequential pacemaker that delivers impulses to the atrium and ventricles on the basis of sensed ventricular and atrial activity, although the latter can only inhibit atrial impulses and cannot trigger ventricular stimulation
• DVI pacemaker : a type of atrioventricular sequential pacemaker that delivers impulses to the atrium and ventricle on the basis of sensed ventricular activity only
• ventricular asynchronous (VOO) pacemaker : an artificial cardiac pacemaker that stimulates the ventricle at a constant rate, without sensing atrial or ventricular activity; rarely used except to initiate or terminate some tachycardias
• ventricular demand inhibited (VVI) pacemaker : an artificial cardiac pacemaker that delivers stimuli to the ventricle at a fixed rate in the absence of sensed ventricular activity; spontaneous cardiac activity causes inhibition of pacemaker output, termination of the current stimulation cycle, and initiation of a new cycle
• ventricular pacing, ventricular sensing, inhibition response, rate-adaptive (VVIR) cardiac pacemaker : a ventricular demand inhibited pacemaker that is responsive to the patient's respiratory rate and thus to exercise and metabolic needs. Damage may occur during mammography^ref
• ventricular demand triggered (VVT) pacemaker : an artificial cardiac pacemaker that delivers stimuli to the ventricle at a fixed rate in the absence of sensed ventricular activity; spontaneous cardiac activity triggers pacemaker output, which falls ineffectively in the myocardial refractory period and initiates a new cycle of pacemaker stimulation
• fixed-rate pacemaker : an artificial cardiac pacemaker set to pace at only a single rate.
• rate responsive pacemaker : an artificial cardiac pacemaker that can deliver stimuli at a rate adjustable to some parameter independent of atrial activity, such as respiratory rate, physical activity level, blood temperature, or mixed venous oxygen saturation level.
• external pacemaker : an artificial cardiac pacemaker located outside the body with output wires connected to circular chest electrodes, with a wire sewn directly into the heart, or with an electrode inserted through an intravenous catheter.
• transthoracic pacemaker : an external cardiac pacemaker delivering stimuli through the chest wall, such as one connected to the heart by percutaneous pacing wires introduced through a transthoracic needle or one in which large electrodes are placed on the skin over the heart.
• implanted or internal pacemaker : an artificial cardiac pacemaker completely implanted into the subcutaneous tissue.
• pacemaker pocket : the subcutaneous area in which the pulse generator and pacing leads of an internal pacemaker are implanted, usually developed in the prepectoralis fascia or the retromammary area
• demand pacemaker : an implanted cardiac pacemaker in which the generator stimulus is inhibited for a set interval (refractory period) by a signal derived from depolarization (normal or ectopic), thus minimizing the risk of pacemaker-induced ventricular fibrillation.
• synchronous pacemaker : an implanted cardiac pacemaker that synchronizes the electromechanical events in the atrium with those of the ventricle by delivering stimuli in response to sensed activity in the atrium, ventricle, or both.
• single chamber pacemaker : an implanted cardiac pacemaker having only one lead, which is placed in either the atrium or the ventricle.
• dual chamber pacemaker : a pacemaker having two leads, one in the atrium and one in the ventricle, so that electromechanical synchrony between the chambers can be approximated.
• unipolar pacemaker : an implanted cardiac pacemaker in which the lead has a single stimulating electrode, the cathode, with the anode connected to an indifferent electrode, usually the outer surface of the pulse generator.
• bipolar pacemaker : an implanted cardiac pacemaker in which the lead contains both electrodes, anode and cathode, and is thus a complete circuit.
• radiofrequency pacemaker : a cardiac pacemaker consisting of an antenna coil on the skin and a subcutaneously implanted receiving coil with an electrode inserted into the ventricular myocardium. Pulses from a lightweight radio transmitter carried by the patient are transmitted to the pacemaker.
• asynchronous pacemaker : an artificial cardiac pacemaker that delivers stimuli at a fixed rate, independent of any atrial or ventricular activity.
• transvenous pacemaker : an artificial cardiac pacemaker, either external or implantable, that is connected to the heart by pacing leads passed through the venous circulation.
Indications : summary of guidelines for permanent pacing (2002 New or Revised Recommendations) (Class I: Evidence that procedure/treatment is indicated; Class IIa: Conflicting evidence but weight of evidence in favor; Class IIb: Efficacy less well established; Class III: Evidence that procedure/treatment is not effective)
• acquired AV block in adults
• class I
• third-degree and advanced second-degree AV block, associated with any one of the following:
• symptomatic bradycardia
• arrhythmias and other conditions that require drugs that result in symptomatic bradycardia
• documented periods of asystole  3.0 s or any escape rate < 40 beats/min
• after catheter ablation of the AV junction
• postoperative AV block that is not expected to resolve
• neuromuscular diseases
• class IIa
• asymptomatic third-degree block with average awake ventricular rates of  40 beats/min
• asymptomatic type II second-degree AV block with a narrow QRS
• asymptomatic type I second-degree AV block at intra- or infra-His levels
• first- or second-degree AV block with symptoms similar to those of pacemaker syndrome
• class IIb
• marked first-degree AV block (> 0.3 s) in patients with LV dysfunction in whom a shorter AV interval results in hemodynamic improvement, presumably by decreasing left atrial filling pressure
• class III
• intermittent third-degree AV block
• asymptomatic type I second-degree AV block at the AV node
• AV block expected to resolve
• chronic bifascicular and trifascicular block
• class I
• intermittent third-degree AV block
• type II second-degree AV block
• alternating bundle-branch block
• class IIa
• syncope when other likely causes have been excluded
• incidental finding at EP study of HV interval  100 ms
• incidental finding at EP study
• class IIb
• neuromuscular diseases
• class III
• fascicular block without AV block or symptoms
• fascicular block with first-degree AV block without symptoms
• after acute myocardial infarction
• class I
• persistent second-degree AV block in the His-Purkinje system with bilateral bundle branch block or third-degree AV block
• transient advanced (second- or third-degree) infranodal AV block and associated bundle branch block
• persistent and symptomatic second- or third-degree AV block
• class IIb : persistent second- or third-degree AV nodal block
• class III
• transient AV block in the absence of intraventricular conduction defects
• transient AV block in the presence of isolated left anterior fascicular block
• acquired left anterior fascicular block in absence of AV block
• persistent first-degree AV block in the presence of old bundle branch block
• sinus node dysfunction
• class I
• with documented symptomatic bradycardia
• symptomatic chronotropic incompetence
• class IIa
• with heart rate < 40 beats/min not associated with symptoms
• with syncope of unexplained origin
• class IIb : with minimal symptoms
• class III
• asymptomatic patients
• in patients with symptoms documented as not associated with a slow heart rate
• with symptomatic bradycardia due to nonessential drug therapy
• pacemakers that automatically detect and pace to terminate tachycardias
• class I
• symptomatic recurrent supraventricular tachycardia that is reducibly terminated by pacing after drugs and catheter ablation failure
• symptomatic recurrent sustained VT as part of an automatic defibrillator system
• pacing recommendations to prevent tachycardia
• class I : sustained pause-dependent VT
• class IIa : high-risk patients with congenital long-QT syndrome
• class IIb
• AV reentrant or AV node reentrant supraventricular tachycardia not responsive to therapy
• prevention of symptomatic, drug-refractory, recurrent atrial fibrillation
• hypersensitive carotid sinus syndrome and neurocardiogenic syncope
• class I
• recurrent syncope caused by carotid sinus stimulation
• minimal carotid sinus pressure induces ventricular asystole of >3 s duration in the absence of any medication that depresses the sinus node or AV conduction
• class IIa
• recurrent syncope without clear, provocative events and with a hypersensitive cardioinhibitory response
• syncope of unexplained origin when major abnormalities of sinus node function or AV conduction are discovered or provoked in electrophysiologic studies
• significantly symptomatic and recurrent neurocardiogenic syncope associated with bradycardia documented spontaneously or at the time of tilt-table testing
• class IIb : neurally mediated syncope with significant bradycardia reproduced by a head-up tilt
• class III :
• hyperactive cardioinhibitory response to carotid sinus stimulation in the absence of symptoms
• recurrent syncope, lightheadedness, or dizziness in the absence of a hyperactive cardioinhibitory response
 Complications :
• runaway pacemaker : a malfunctioning artificial cardiac pacemaker that abruptly accelerates its pacing rate, resulting in pacemaker-induced ventricular tachycardia.
• twiddler's syndrome : dislodgement, breakdown, or other malfunction of an artificial cardiac pacemaker, chemotherapy port, drip infusion valve, or similar implanted diagnostic or therapeutic device as a result of unconscious or habitual manipulation by the patient.
• pacemaker twiddler's syndrome : twiddler's syndrome in a patient with an artificial cardiac pacemaker.
• alternating currents (A.C.)
• low frequency (< 100,000 Hz)
• defibrillation : termination of atrial fibrillation (AF) or ventricular fibrillation (VF). One patient with a defibrillator describes the jolt delivered by today's devices as "like being kicked in the chest - it's certainly not very pleasant". Defibrillation is currently a crude technique, which delivers an electric current of between 3 and 10 J of energy to disrupt the rogue waves and shock the heart back into its normal activity. Roughly 175,000 people around the world have a defibrillator fitted inside their chest every year: the first was fitted in 1980. The devices are usually fitted just below the sternum, with electrical leads going into the heart. > 80% of patients fitted with defibrillators have already had a heart attack. Heart attacks increase the risk of fibrillation because they leave scars of dead tissue inside the heart, which have a higher electrical resistance than the surrounding tissue. This allows rotating electrical waves to develop around these areas. By timing the shock so that it arrives just as the wave is passing around the scar tissue, it is possible to dislodge and quench the electrical tornado using only 0.5 J of energy - so little that a patient would barely notice it. The approach works because scar tissue is more susceptible to electric shocks, so a small pulse affects only the scar, not the surrounding cells. If the electrical pulse is applied at just the right time, it dislodges the wave from the scar tissue. Once freed into the surrounding healthy tissue, the wave can no longer sustain itself and dies away. Efimov has tested the idea in rabbit hearts, and managed to defibrillate them with < 20% of the energy that is normally required^ref. Using less energy will avoid problems caused by conventional defibrillators, which can make tiny holes in the membranes of heart cells : most of these holes repair themselves, but it can be dangerous for patients who already have the most damaged hearts. But the most important benefit for patients could be a psychological one. If less energy were required, manufacturers could also make the devices much smaller. Defibrillators are currently around the size of a packet of cigarettes, not insignificant for a device that is implanted into the chest. If this works out, it could make a defibrillator the same size as a pacemaker - that's about a fifth the size
• at a frequency slightly less than the rate at which the spiral wave normally turns, the chaos is quieted, making the scrolls shrink and disappear. A greater-than-normal frequency makes stable scrolls expand and become turbulent.
• paddles at 110 V (alternated current with n = 60 Hz) for 100 ms. It induces a contemporaneous depolarization in whole myocardium, followed by a contemporaneous refractariety, which causes cardiac standstill for 3-5". When the SA node restarts pacemaking, the ectopic focus can or cannot be still active.
• high frequency (> 100,000 Hz)
• diathermy : heating of the body tissues due to their resistance to the passage of high-frequency electromagnetic radiation, electric currents, or ultrasonic waves
• thermotherapy : treatment of disease by the application of heat; usually defined as that which raises body temperature to above 45° C.
• medical diathermy / thermopenetration : application of currents of low tension and high amperage, which produce warmth in the deeper parts of the body; used particularly to promote muscle relaxation and to treat joint disorders including contractures
• microwave diathermy : medical diathermy using electromagnetic radiation by microwaves; it heats to a greater tissue depth than short-wave diathermy and is particularly effective in heating tissues with high water content such as muscles, subcutaneous fat, and fluid-filled cavities.
• ultrashort wave diathermy : diathermy in which the wavelength used is < 10 m
• ultrasound diathermy : medical diathermy using ultrasound; it heats to a tissue depth of 5 to 6 cm and is particularly used to warm areas around tissue interfaces such as joints.
• radiathermy / short wave diathermy or therapy (a.k.a. marconiterapia in Italy) : the therapeutic heating of the body tissues by means of an oscillating electromagnetic field of high frequency; the frequency varies from 10 million to 100 million Hz and the wavelength from 30 to 3 m; it heats to a tissue depth of 2 to 3 cm and is used for heating large areas of body surface
• radartherapy : wavelength from 1 mm to 1 m
• surgical diathermy / electrocoagulation : coagulation of tissue usually by means of an electrocautery with a biterminal high frequency electric current
• thermocoagulation : coagulation of tissue by the action of high-frequency currents; used in removal of growths and in stereotactic surgery.
• radiofrequency thermocoagulation : the use of electromagnetic waves in the radio frequency range to coagulate tissue in stereotactic surgery and rhizotomy

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