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Shock defibrillator

Schron EB, Exner DV, Yao Q, et al. Quality of life in the antiarrhythmics versus implantable defibrillators trial impact of therapy and influence of adverse symptoms and defibrillator shocks. Circulation. Feb 5 2002 105(5) 589-594. [Pg.48]

Some patients are at risk of a form of arrhythmia called fibrillation, which is a completely uncoordinated, quivering, nonfunctional heartbeat. If not corrected quickly, fibrillation can cause death. Since 1985, pacemakers have been available to monitor the speed of the heart and deliver an appropriate electrical shock to the heart muscle if it begins to fibrillate. The device can deliver a low-level pacing shock, an intermediate shock, or a jolting, defibrillating shock if necessary. [Pg.724]

Pacifico A, Hohnloser SH, WilUams JH, et al. Prevention of implantable-defibrillator shocks by treatment with sotalol. N Engl J Med 1999 340 1855-1862. [Pg.355]

Daubert JP, Wojciech Z, Cannom DS, et al. Inappropriate implantable cardioverter defibrillator shocks in MADIT II. J Am Coll Cardiol 2008 51(14) T357-65. [Pg.18]

Fig 1 41 Section of interventricular septum from a patient who underwent cardiac transplantation 676 days after implantable cardioverter-defibrillator lead implantation and 7 days after last defibrillator shock (a). Right ventricular surface of interventricular septum (R) is at the top and left ventricular surface (L) at bottom. Characteristic fibroelastic tissue encircles the lead curved arrow). Trichrome-stained section of tissue (b) band of fibroelastic tissue curved arrow) encircles lead (L), and beneath, in myocardium, lies fibrous connective tissue F). Area of confluent fibrous connective tissue immediately adjacent to lead also extends into surrounding myocardium, forming radial pattern of interstitial fibrosis arrows), suggesting that shocks have caused lines of electrical injury (courtesy [51])... [Pg.29]

The patient is defibriUated while coupled to the amplifier. A defibrillator shock can be up to 5 kV and is applied via two large electrodes to the thorax. A substantial part of this voltage can appear between PUl and PU2. The frequency is much lower and the LPFs will damp the signal much less than the static discharge case. But file protection diodes will play an important role. [Pg.290]

Defibrillator shocks are the largest electric shocks used in clinical medicine, up to 50 A is applied for some milliseconds through the thorax, driven by approximately 5 kV. The... [Pg.450]

Cardiovascular Torsade de pontes has been attributed to cisapride 10 mg tds in a 36-year-old woman, in association with low serum potassium and magnesium concentrations [S ]. She had recurrent episodes, which required 50-70 defibrillation shocks per day, while several antidysrhyth-mic agents, including bretylium, phenytoin, isoprenaline, amiodarone, lidocaine, and magnesium sulfate, were ineffective. When cisapride was withdrawn the episodes of torsade de pointes resolved within a day. [Pg.556]

Hussain A, Ghazal S. After more than 300 defibrillation shocks, patient still alive 12 years later refractory torsade de pointes due to polypharmacy and persistent vomiting. J Saudi Heart Ass 2010 22 149-51. [Pg.573]

The basic biopotential amplifier described above, along with the specific design considerations for each biopotential, can yield a signal acquisition of acceptable quality in most laboratory settings. In practice, however, further enhancements are always necessary to achieve acceptable clinical performance in novel applications. These enhancements include circuits for reducing electric interference, filtering noise, reduction of artifacts, electrical isolation of the amplifier, and electrical protection of the circuit against defibrillation shocks [9]. [Pg.567]

Initiating factors, often multifactorial, include ectopic beats, ischemia, alteration in conduction or refractoriness, electrolyte disturbances, drugs, and autonomic perturbations. Factors that result in sudden death because of a ventricular arrhythmia are complex and understood poorly. Any simphstic medical approach that alters the arrhythmic substrate (such as drug therapy or even catheter ablation) may fail to reduce risk and may make things worse. Alternatively, a defibrillation shock, timed properly, can stop ventricular fibrillation. [Pg.496]

Guamieri T, Datorre SD, Bondke H, Brinker J, Myers S, Levine JH. Increased pacing threshold after an automatic defibrillator shock in dogs effect of class I and class II antiarrhythmic drugs. Pacing Clin Electrophysiol 1988 11 1324-1330. [Pg.591]

Chan NY, Ho LWL. Inappropriate implantable cardioverter-defibrillator shock dne to external alternating current leak Report of two cases. Europace 2005 7 193-196. [Pg.618]

Vlay SC. Fish pond electromagnetic interference resulting in an inappropriate implantable cardioverter defibrillator shock. Pacing Clin Electmphysiol 2002 25 1532. [Pg.618]

Ventricular tachyarrhythmia therapy in an ICD may be programmed for each zone of detection. For arrhythmias detected in the VF zone this occurs in the form of defibrillation. Shocks to terminate tachycardias in this zone may occur regardless of the timing in the cardiac cycle, and up to a maximum of 25-42 J stored energy in contemporary devices. Some ICD models may deliver up to eight shocks per arrhythmia episode. [Pg.80]

The timing of a defibrillation shock necessarily delivered with... [Pg.80]

Siu CW, Tse HF, Lau CP. Inappropriate implantable cardioverter defibrillator shock from a transcutaneous muscle stimulation device therapy. J Interv Card Electrophysiol 2005 13(1) 73-75. [Pg.162]


See other pages where Shock defibrillator is mentioned: [Pg.128]    [Pg.128]    [Pg.244]    [Pg.584]    [Pg.222]    [Pg.227]    [Pg.234]    [Pg.242]    [Pg.318]    [Pg.322]    [Pg.465]    [Pg.556]    [Pg.356]    [Pg.358]    [Pg.495]    [Pg.38]    [Pg.245]    [Pg.623]   
See also in sourсe #XX -- [ Pg.45 , Pg.450 , Pg.452 ]




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