Skip to main content
SpringerLink
Log in

Mechanismen der elektrischen Defibrillation

Mechanisms of electrical defibrillation

  • Themenübersicht
  • Published:
Herzschrittmachertherapie und Elektrophysiologie Aims and scope Submit manuscript

Zusammenfassung

Kammerflimmern wurde als “chaotische, zufällige asynchrone elektrische Aktivität der Herzkammern aufgrund sich wiederholender kreisender Erregungen und/oder schneller, fokaler Entladungen” beschrieben. Bei der Entstehung von Kammerflimmern sind Reentry- und Nichtreentry-Mechanismen beteiligt. Aufrechterhalten wird Kammerflimmern von multiplen, disorganisierten, wandernden Erregungsfronten, die ihre Ausbreitungsrichtung ständig ändern. Die elektrische Defibrillation ist die derzeit einzig verfügbare Therapie zur Beendigung von Kammerflimmern. Während der Defibrillation wird ein elektrischer Schock auf das Herz appliziert. Dieser Schock muß stark genug sein, um das Kammerflimmern zu beenden, darf aber andererseits nicht so stark sein, daß er das Myokard schädigt. Das Verständnis des Defibrillationsmechanismus ist besonders durch die klinische Anwendung des implantierbaren Kardioverter/Defibrillators gewachsen.

Die Entwicklung neuer Schockformen, Elektrodenkonfigurationen und Elektroden für immer kleinere, langlebige Geräte setzt ein besseres Verständnis der Vorgänge bei der Defibrillation voraus. Die Entwicklung von computergesteuerten elektrischen und optischen Mapping-Systemen, Mikroelektroden-Techniken und mathematischen Modellen schuf die Voraussetzung für die Erforschung der bei der Defibrillation ablaufenden Vorgänge.

Ein Defibrillations-Schock wirkt auf Herzmuskelzellen, die sich in unterschiedlichen Phasen ihres Aktionspotentials befinden. Dabei werden (1) Zellen direkt erregt, (2) eine “graded response” erzeugt oder (3) kein Effekt erzielt. “Graded response” resultiert in einer Verlängerung des Aktionspotentials und damit der Refraktärphase. Die Verlängerung der Refraktärphase ist entscheidend für den Defibrillationserfolg. Mapping-Studien zeigen, daß für eine erfolgreiche Defibrillation ein bestimmter minimaler Potential-Gradient im Ventrikelmyokard erzeugt werden muß. Für gebräuchliche monophasische Schocks beträgt dieser Gradient 5–7 V/cm (in Abhängigkeit von der Schockform und der Orientierung der Myofibrillen).

Es gibt verschiedene Hypothesen, um die Mechanismen zu erklären, die bei einer erfolgreichen Defibrillation ablaufen. Das Für und Wider dieser Hypothesen wird anhand der Ergebnisse experimenteller Studien diskutiert. Die Theorie des “Upper limit of vulnerability” Mechanismus der Defibrillation geht davon aus, daß ein erfolgreicher Defibrillations-Schock existierende Aktivierungsfronten stoppen muß, indem er das Myokard vor diesen Aktivierungsfronten direkt erregt oder die Refraktärphasen verlängert. Dabei dürfen keine neuen Aktivierungsfronten an der Grenze des direkt aktivierten Myokards erzeugt werden. Bei einer Defibrillations-Energie, die zu gering ist, um erfolgreich defibrillieren zu können, entsteht ein “critical point”, an dem ein kritischer Potential-Gradient auf eine kritische Refraktärität trifft. Daraus entsteht eine neue Aktivierungsfront, die in Kammerflimmern degeneriert. Ergebnisse vieler Mapping-Studien unterstützen die “Upper limit of vulnerability” Hypothese der Defibrillation, dennoch lassen sich nicht alle erfolglosen Defibrillations-Schocks mit dieser Theorie erklären.

Klinische Daten und experimentelle Ergebnisse zeigen, daß biphasische Schocks eine niedrigere Defibrillationsschwelle haben als bei Defibrillation mit monophasischen Schockformen. Der genaue Mechanismus, warum biphasische Schocks besser defibrillieren, ist zum jetzigen Zeitpunkt nicht bekannt. Es werden einige Theorien über die höhere Effektivität biphasicher Defibrillations-Schocks vorgestellt.

Summary

Ventricular fibrillation has been described as a “chaotic, random, asynchronous electrical activity of the ventricles due to repetitive reentrant excitation and/or rapid focal discharge”. Reentrant and non-reentrant mechanisms are responsible for the initiation of ventricular fibrillation. After fibrillation has been induced, it is thought that multiple, disorganized, wandering wavelets follow constantly changing reentrant pathways. Electrical defibrillation is the only valid therapeutic approach for ventricular fibrillation. A successful defibrillation shock must be of sufficient strength to stop fibrillation but must not be so strong that damage to the myocardium occurs. The clinical use of the implantable cardioverter/defibrillator device has significantly stimulated research in the field of cardiac defibrillation. In order to develop more efficient shock waveforms and electrode configurations for smaller, and also longer lasting devices, we need a better understanding of the basic mechanisms of defibrillation. The development of computerized electrical mapping systems, capable of recording before, during and after a defibrillation shock, optical recording systems and microelectrodes, for action potential recording before and after the shock application and mathematical models have contributed much to the understanding of defibrillation mechanisms.

An electrical shock hits the cardiac cells in different phases of their action potential. This results in 1) direct activation, 2) a “graded response”, or 3) no effect. “Graded response” produces prolongation of the action potential and prolongs refractoriness without giving rise to a propagated activation front. Refractory period prolongation in an area that is still refractory at the time of the shock is critical for successful defibrillation. Mapping studies have shown that for successful defibrillation with monophasic shocks a minimal potential gradient of 5–7 V/cm is necessary (the exact value depends on the waveform and the orientation of the cells with respect to the electric field).

Several hypotheses have been developed in order to explain the mechanisms that underlie successful defibrillation shocks. This paper will discuss the various theories. The “upper limit of vulnerability” hypothesis for defibrillation states that a successful defibrillation shock must stop existing activation fronts by directly exciting or by prolonging refractoriness just in front of the upcoming activation fronts and must not give rise to new activation fronts at the border of the directly excited area. Shocks slightly weaker then necessary to defibrillate stop fibrillation activation fronts, but give rise to new activation fronts that reinitiate fibrillation. These new activation fronts arise at a “critical point,” where a critical shock potential gradient interferes with a critical degree of tissue refractoriness. Mappping studies support the “upper limit of vulnerability” hypothesis of defibrillation but not all defibrillation failures, however, can be explained by this hypothesis.

Clinical data and experimental results have shown that biphasic shocks may have lower defibrillation thresholds than monophasic shocks. The advantage of defibrillation with a biphasic waveform is not yet clearly understood. We discuss some possible reasons why some biphasic waveforms have lower defibrillation thresholds than monophasic waveforms.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Log in via an institution

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Institutional subscriptions

Literatur

  1. Allessie MA, Bonke FIM, Schopman FJG (1973) Circus movement in rabbit atrial muscle as a mechanism of tachycardia. Cir Res 33:54–62

    CAS  Google Scholar 

  2. Allessie MA, Bonke FIM, Schopman FJG (1976) Circus movement in rabbit atrial muscle as a mechanism of tachycardia: II. The role of nonuniform recovery of excitability in the occurrence of unidirectional block, as studied with multiple microelectrodes. Circ Res 39:168–177

    PubMed  CAS  Google Scholar 

  3. Allessie MA, Bonke FIM, Schopman FJG (1977) Circus movement in rabbit atrial muscle as a mechanism of tachycardia: III. The “leading circle” concept: A new model of circus movement in cardiac tissue without the involvement of an anatomical obstacle. Circ Res 41:9–18

    PubMed  CAS  Google Scholar 

  4. Bardou AL, Degode J, Birkui PJ et al (1988) Reduction of energy required for defibrillation by delivering shocks in orthogonal directions in the dog. PACE 11:1990–1995

    PubMed  CAS  Google Scholar 

  5. Bardy GH, Ivey TD, Allen MD et al (1989) A prospective randomized evaluation of biphasic versus monophasic waveform pulses on defibrillation efficacy in humans. J Am Coll Cardiol 14:728–733

    PubMed  CAS  Google Scholar 

  6. Bardy GH, Ivey TD, Allen MD et al (1989) Evaluation of electrode polarity on defibrillation efficacy. Am J Cardiol 63:433–437

    Article  PubMed  CAS  Google Scholar 

  7. Blanchard SM, Johnson EE, Ideker RE (1994) Myocardial activation at the onset and during ventricular fibrillation. In: Akbtar M, Myerburg RJ, Ruskin JN (Hrsg) Sudden cardiac death. Prevalence, Mechanisms and approaches to diagnosis and treatment. Williams & Wilkins, Malvern, PA, pp 128–143

    Google Scholar 

  8. Chapman PD, Vetter JW, Souza JJ et al (1989) Comparison of monophasic with single and dual capacitor biphasic waveforms for nonthoracotomy canine internal defibrillation. J Am Coll Cardiol 14:242

    PubMed  CAS  Google Scholar 

  9. Chapman PD, Wetherbee JN, Vetter JW et al (1988) Strength duration curves of fixed pulse with variable tilt truncated exponential waveforms for nonthoracotomy internal defibrillation in dogs. PACE 11:1045

    PubMed  CAS  Google Scholar 

  10. Chen PS, Shibata N, Dixon XG et al (1986) Activation during ventricular fibrillation in open-chest dogs: evidence of complete cessation and regeneration of ventricular fibrillation after unsuccessful shocks. J Clin Invest 77:810

    Article  PubMed  CAS  Google Scholar 

  11. Chen PS, Shibata N, Dixon EG et al (1986) Comparison of the defibrillation threshold and the upper limit of ventricular vulnerability. Circulation 73:1022–1028

    PubMed  CAS  Google Scholar 

  12. Chen PS, Wolf PD, Claydon FJ III et al (1986) The potential gradient field created by epicarial defibrillation electrodes in dogs. Circulation 74:354–365

    Google Scholar 

  13. Chen PS, Wolf PD, Ideker RE (1991) Mechanism of cardiac defibrillation. A different point of view. Circulation 84:913–919

    PubMed  CAS  Google Scholar 

  14. Chen P-S, Wolf Pd, Melnick SB et al (1990) Comparison of ventricular activation during ventricular fibrillation and following unsuccessful defibrillation shocks in open chest dogs. Circ Res 66:1544–1560

    PubMed  CAS  Google Scholar 

  15. Claydon FJ III, Pilkington TC, Tang ASL et al (1988) A volume conductor model of the thorax for the study of defibrillation fields. IEEE Trans Biomed Eng BME-35:981–992

    Article  Google Scholar 

  16. Cooper RAS, Wallenius ST, Smith WM et al (1993) The effect of phase separation on biphasic waveform defibrillation. PACE 16:471

    PubMed  CAS  Google Scholar 

  17. Davy JM, Fain ES, Dorian P, Winkle RA (1987) The relationship between successful defibrillation and delivered energy in open-chest dogs: repappraisal of the “defibrillation threshold” concept. Am Heart J 113:77–84

    Article  PubMed  CAS  Google Scholar 

  18. Deale OC, Wesley RC Jr, Morgan D, Lerman BB (1990) Nature of defibrillation: determinism versus probabilism. Am J Physiol 259:H1544-H1550

    PubMed  CAS  Google Scholar 

  19. Dillon SM (1991) Optical recordings in the rabbit heart show that defibrillation stregth shocks prolong the duration of depolarization and the refactory period. Circ Res 69:842–856

    PubMed  CAS  Google Scholar 

  20. Dillon SM (1992) Synchronized repolarisation after defibrillation shocks: a possible component of the defibrillation process demonstrated by optical recordings in rabbit heart. Circulation 85:1865–1878

    PubMed  CAS  Google Scholar 

  21. Dixon EG Tang ASL, Wolf PD et al (1987) Improved defibrillation thresholds with large contoured epicardial electrodes and biphasic waveforms. Circulation 76:1176

    PubMed  CAS  Google Scholar 

  22. Echt DS, Armstrong K, Schmidt P et al (1985) Clinical experience, complications and survival in 70 patients with the automatic implantable cardioverter/defibrillator. Circulation 71:289–296

    PubMed  CAS  Google Scholar 

  23. Fahey JB, Kim Y, Ananthaswamy A (1987) Optimal electrode configurations for external cardiac paicng and defibrillation: an inhomogeneous study. IEEE Trans Biomed Eng BME-34:743–748

    Article  Google Scholar 

  24. Feeser SA, Tang ASL, Kavanagh KM et al (1990) Stregth-duraction and probability of success curves for defibrillation with biphasic waveforms. Circulation 82:2128–2141

    PubMed  CAS  Google Scholar 

  25. Frazier DW, Krassowska W, Chen PS et al (1988) Extracellular field required for excitation in three-dimensional anisotropic canine myocardium. Circ Res 63:147–164

    PubMed  CAS  Google Scholar 

  26. Frazier DW, Wolf PD, Wharton JM et al (1989) Stimulus-induced critical point: mechanism of electrical initiation of reentry in normal canine myocardium. J Clin Invest 83:1039–1052

    Article  PubMed  CAS  Google Scholar 

  27. Geddes LA, Tacker WA Jr (1971) Engineering and physiological considerations of direct capacitor-discharge ventricular defibrilation. Med Biol Eng 9:185–199

    Article  PubMed  CAS  Google Scholar 

  28. Henriquez CS (1993) Simulating the electrical behavior of cardiac tissue using the bidomain model. Crit Rev Biomed Eng 21:1

    PubMed  CAS  Google Scholar 

  29. Ideker RE, Klein GJ, Harrison L et al (1981) The transition to ventricular fibrillation induced by reperfusion following acute ischemia in the dog: A period of organized epicardial activation. Circulation 63:1371–1379

    PubMed  CAS  Google Scholar 

  30. Ideker RE, Tang ASL, Frazier DW et al (1991) Ventricular defibrillation: basic concepts. In: El-Sharif N, Samet P (Hrsg) Cardiac pacing and electrophysiology. W. B. Saunders Co. Orlando, FL, p 713

    Google Scholar 

  31. Ideker RE, Tang ASL, Frazier DW et al (1991) Basic mechanisms of ventricular defibrillation. In: Glass L, Hunter P, Mc Golloch A (Hrsg) Theory of the heart. Springer-Verlag, New-York, pp 533–560

    Google Scholar 

  32. Irnich W (1994) Defibrillation theory and its clinical impact. In: Singer I (Hrsg) Implantable cardioverter-defibrillator. Futura Publishing Comp, Inc. Armonk, NY, pp 135–152

    Google Scholar 

  33. Janse MJ, van Capelle FJL, Morsink H et al (1980) Flow of “injury” current patterns of excitation during early ventricular arrhythmias in acute regional myocardial ischemia in isolated porcine and canine hearts: Evidence for two different arrhythmogenic mechanisms. Circ Res 47:151–165

    PubMed  CAS  Google Scholar 

  34. Jones JL (1994) Ventricular Fibrillation. In: Singer I (Hrsg) Implantable cardioverter-defibrillator. Future Publishing Comp, Inc., Armonk, NY, pp 43–67

    Google Scholar 

  35. Jones JL, Jones RE (1991) Threshold reduction with biphasic defibrillator waveforms: Role of excitation channel recovery in computer model of the ventriclar action potential. J Electrocardiol 23:30–35

    Article  Google Scholar 

  36. Jones JL, Jones RE, Balasky G (1987) Improved cardiac cell excitation with symmetrical biphasic defibrillator waveforms. Am J Physiol 253:H1418-H1424

    PubMed  CAS  Google Scholar 

  37. Jones JL, Jones RE, Milne KB (1994) Refractory period prolongation by biphasic defibrillator waveforms is associated with enhanced sodium current in a computer model of the ventricular action potential. IEEE Trans Biomed Eng 41:60–68

    Article  PubMed  CAS  Google Scholar 

  38. Jones DL, Klein GJ, Guiraudon GM et al (1986) Interalcardiac defibrillation in man: pronounced improvement with sequential pulse delivery to two different lead orientations. Circulation 73: 484–491

    PubMed  CAS  Google Scholar 

  39. Jones DL, Klein GJ, Guiraudon GM et al (1988) Prediction of defibrillation success from a single defibrillation threshold measurement with sequential pulses and two current pathways in humans. Circulation 78:1144–1149

    PubMed  CAS  Google Scholar 

  40. Jones DL, Klein GJ, Kallok MJ (1985) Improved internal defibrillation with twin pulse sequential energy delivery to different lead orientations in pigs. Am J Cardiol 55:821–825

    Article  PubMed  CAS  Google Scholar 

  41. Jones DL, Klein GJ, Rattes MF et al (1988) Internal cardiac defibrillation: single and sequential pulses and a variety of lead orientations. PACE 11: 583–591

    PubMed  CAS  Google Scholar 

  42. Jones JL, Lepeschkin E, Jones RE, Rush S (1978) Response of cultured myocardial cell to countershock-type electric field stimulation. Amer J Physiol 235:H214-H222

    PubMed  CAS  Google Scholar 

  43. Jones JL, Swartz JF, Jones RE et al (1990) Increasing fibrillation duration enhances relative asymmetrical biphasic versus monophasic defibrillator waveform efficacy. Circ Res 67:376–384

    PubMed  CAS  Google Scholar 

  44. Kao CY, Hoffman BF (1958) Graded and decremental response in heart muscle fibers. Am J Physiol 194:187–196

    PubMed  CAS  Google Scholar 

  45. Klee M, Plonsey R (1976) Stimulation of spheroidal cellsthe role of cell shape. IEEE Trans Biomed Eng BME-23: 347–354

    Article  CAS  Google Scholar 

  46. Knisley SB, Blitchington TF, Hill BC et al (1993) Optical measurements of transmembrane potential changes during electric field stimulation of ventricular cells. Circ Res 72:255

    PubMed  CAS  Google Scholar 

  47. Knisley SB, Smith WM, Ideker RE (1992) Effect of field stimulation on cellular repolarization in rabbit myocardium: implications for reentry induction. Circ Res 70:707–715

    PubMed  CAS  Google Scholar 

  48. Knisley SB, Smith WM, Ideker RE et al (1992) Effect of intrastimulus polarity reversal on electric field stimulation thresholds in frog and rabbit myocardium. J Cardiovasc Electrophysiol 3:239

    Article  Google Scholar 

  49. Kothiyal KP, Shankar B, Fogelson LJ, Thakor NV (1988) Three-dimensional computer model of electric fields in internal defibrillation. Proc IEEE 76:720–730

    Article  Google Scholar 

  50. Krassowska W, Frazier DW, Pilkington TC et al (1990) Potential distribution in three-dimensional periodic myocardium. Part II. Application to extracellular stimulation. IEEE Trans Biomed Eng 37:267

    Article  PubMed  CAS  Google Scholar 

  51. Li HG, Jones DL, Yee R, Klein GJ (1993) Defibrillation shocks produce different effects on purkinje fibers and ventricular muscle: implications for successful defibrillation, refibrillation and postshock arhythmia. J Am Coll Cardiol 22:607–614

    PubMed  CAS  Google Scholar 

  52. Mirowski M, Mower MM, Reid PR et al (1982) The automatic implantable defibrillator. PACE 5:384–401

    PubMed  CAS  Google Scholar 

  53. Moe GK, Abildskov JA (1959) Atrial fibrillation as a self-sustaining arrhythmia independent of focal discharge. Am Heart J 58:59

    Article  PubMed  CAS  Google Scholar 

  54. Mower MM, Mirowski M, Spear JF, Moore EN (1974) Patterns of ventricular activity during catheter defibrillation. Circulation 49:858–861

    PubMed  CAS  Google Scholar 

  55. O’Neill PG, Boahene KA, Lawrie GM et al (1991) The automatic implatable cardioverter-defibrillator: effect of patch polarity on defibrillation threshold. J Am Coll Cardiol 17:707–711

    PubMed  Google Scholar 

  56. Peleska B (1963) Cardiac arrhythmias following condenser discharges and their dependence upon strength of current and phase of cardiac cycle. Circ Res 13:21

    PubMed  CAS  Google Scholar 

  57. Plonsey R, Barr RC, Witkowski FX (1991) One-dimensional model of cardiac defibrillation. Med Biol Eng Comput 29:465

    Article  PubMed  CAS  Google Scholar 

  58. Pogwizd SM, Corr PB (1987) Electrophysiologic mechanisms underlying arrhythmias due to reperfusion of ischemic myocardium. Circulation 76: 404–426

    PubMed  CAS  Google Scholar 

  59. Pogwizd SM, Corr PB (1990) Mechanisms underlying the development of ventricular fibrillation during early myocardial ischemia. Circ Res 66:672–695

    PubMed  CAS  Google Scholar 

  60. Ramirez IF, Isenberg SR, Lehr JL, Schoen FJ (1989) Effects of cardiac configuration, paddle placement and paddle size on defibrillation current distribution: a finite element model. Med Biol Eng Comp 27:587–594

    Article  Google Scholar 

  61. Rush S, Lepeschkin E, Grgoritsch A (1969) Current distribution from defibrillation electrodes in a homogeneous torso model. J Electrocardiol 2: 331–341

    Article  PubMed  CAS  Google Scholar 

  62. Saksena S, Scott SE, Accorti PR et al (1990) Efficacy and safety of monophasic and biphasic waveform shocks using a braided endocardial defibrillation lead system. Am Heart J 120:1342

    Article  PubMed  CAS  Google Scholar 

  63. Schuder JC, Stoeckle H, Gold JH et al (1970) Experimental ventricular defibrillation with an automatic and completely implanted system. Trans Am Soc Artif Intern Organs 16:207–212

    PubMed  CAS  Google Scholar 

  64. Schuder JC, Stoeckle H, Keskar PY et al (1970) Transthoracic ventricular defibrillation in the dog with unidirectional rectangular double pulse. Cardiovasc Res 4:497–501

    Article  PubMed  CAS  Google Scholar 

  65. Schuder JC, Stoeckle H, Mc Daniel WC, Dbeis M (1987) Is the effectiveness of cardiac ventricular defibrillation dependent upon polarity? Med Instrum 21:262–265

    PubMed  CAS  Google Scholar 

  66. Sepulveda NG, Roth BJ, Wikswo JP Jr (1989) Current injection into a two-dimensional anisotropic bidomain. Biophys J 55:987

    Article  PubMed  CAS  Google Scholar 

  67. Sepulveda NG, Wikswo JP Jr, Echt DS (1990) Finite element analysis of cardiac defibrillation current distributions. IEEE Trans Biomed Eng BME-37: 354–365

    Article  CAS  Google Scholar 

  68. Shibata N, Chen PS, Dixon EG et al (1988) Epicardial activation following unsuccessful defibrillation shocks in dogs. Am J Physiol 255:H902-H909

    PubMed  CAS  Google Scholar 

  69. Swartz JF, Jones JL, Jones RE, Fletcher R (1991) Conditioning prepulse of biphasic defibrillator waveforms enhances refractoriness to defibrillation wavefronts. Circ Res 68:438–449

    PubMed  CAS  Google Scholar 

  70. Sweeney RJ, Gill RM, Steinberg MI, Reid PR (1990) Ventricular refractory period extension caused by defibrillation shocks. Circulation 82:965–972

    PubMed  CAS  Google Scholar 

  71. Tang ASL, Wolf PD, Afewoek Y et al (1992) Three-dimensional potential gradient fields generated by intracardiac catheter and cutaneous patch electrodes. Circulation 85:1857–1864

    PubMed  CAS  Google Scholar 

  72. Tang ASL, Yabe S, Wharton JM et al (1989) Ventricular defibrillation using biphasic waveforms: the importance of phase duration. J Am Coll Cardiol 13:207

    Article  PubMed  CAS  Google Scholar 

  73. Tchou PJ, Kadri N, Anderson J et al (1988) Automatic implantable cardioverter defibrillators and survival of patients with left ventricular dysfunction and malignant ventricular arrhythmias. Ann Intern Med 109:529–534

    PubMed  CAS  Google Scholar 

  74. Tovar O et al (1994) Correlation between shock induced response duration and defibrillation. Proc Ann Int Conf IEEE Eng Med Biol Soc 16:21–22

    Article  Google Scholar 

  75. Trayanova NA, Pilkington TC, Henriquez CS (1991) A periodic bidomain model for cariac tissuee. In: Nagel JH, Smith WM (Hrsg) Proceedings of the 13th Annual Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, Inc., Orlando, FL, p 502

    Chapter  Google Scholar 

  76. Tung L (1996) Detrimental Effects of Electrical Fields on Cardiac Muscle. Proceedings of the IEEE 84:366–378

    Article  CAS  Google Scholar 

  77. van Vleet JF, Tacker WA Jr, Geddes LA, Ferrans VJ (1978) Sequential cardiac morphologic alterations induced in dogs by single tranthoracic damped sinusoidal waveform defibrillator shocks. Am J Vet Res 39:271

    PubMed  Google Scholar 

  78. Walcott GP, Walcott KT, Knisley SB et al (1994) Mechanisms of defibrillation for monophasic and biphasic waveforms. PACE 17:478–498

    PubMed  CAS  Google Scholar 

  79. Wharton JM, Richard VJ, Murry CE Jr et al (1990) Electrophysiological effects on monophasic and biphasic stimuli in normal and infarcted dogs. PACE 13:1158

    PubMed  CAS  Google Scholar 

  80. Wharton JM, Wolf PD, Smith WM et al (1992) Cardiac potential and potential gradient fields generated by single, combined, and sequential shocks during ventricular defibrillation. Circulation 85:1510

    PubMed  CAS  Google Scholar 

  81. Wiggers CJ (1940) The physiologic basis for cardiac resuscitation from ventricular fibrillation: method for serial defibrillation. Am Heart J 20:413

    Article  Google Scholar 

  82. Windisch H, Ahammer H, Schaffer P et al (1990) Optical monitoring of excitation patterns in single cardiomyocytes. Proceedings of the 12th Annual Conference of the IEEE Engineering in Medicine and Biology Society 12:1641

    Google Scholar 

  83. Winkle RA, Mead RH, Ruder MA et al (1989) Improved low energy defibrillation efficacy in man with the use of a biphasic truncated exponential waveform. Am Heart J 117:122–127

    Article  PubMed  CAS  Google Scholar 

  84. Winkle RA, Mead RH, Ruder MA et al (1989) Long-term outcome with the automatic implantable cardioverter-defibrillator. J Am Coll Cardiol 13: 1353–1361

    Article  PubMed  CAS  Google Scholar 

  85. Witkowski FX, Kerber RE (1991) Currently known mechanisms underlying direct current external and internal cardiac defibrillation. J Cardiovasc Electrophysiol 2:262

    Article  Google Scholar 

  86. Witkowski FX, Penkoske PA, Plonsey R (1990) Mechanism of cardiac defibrillation in open-chest dogs with unipolar DC-coupled simultaneous activation and shock potential recordings. Circulation 82:244–260

    PubMed  CAS  Google Scholar 

  87. Wyse DC, Kavanagh KM, Gillis AM et al (1993) Comparison of biphasic and monophasic shocks for defibrillation using a nonthoracotomy system. Am J Cardiol 71:197

    Article  PubMed  CAS  Google Scholar 

  88. Yabe S, Smith WM, Daubert JP et al (1990) Conduction disturbances caused by high current density electric fields. Circ Res 66:1190

    PubMed  CAS  Google Scholar 

  89. Zhou X, Daubert JP, Wolf PD et al (1993) Epicardial mapping of ventricular defibrillation with monophasic and biphasic shocks in dogs. Circ Res 72:145–160

    PubMed  CAS  Google Scholar 

  90. Zhou X, Knisley SB, Wolf PD et al (1990) Prolongation of repolarization time by electric field stimulation with monophasicand biphasic shocks in open chest dogs. Circ Res 68:1761

    Google Scholar 

  91. Zhou X, Wolf PD, Rollins DL et al (1993) Effects of monophasic and biphasic shocks on action potential duration during ventricular fibrillation in dogs. Circ Res 73:325

    PubMed  CAS  Google Scholar 

  92. Zipes DP (1975) Electrophysiological mechanisms involved in ventricular fibrillation. Circulation 51:III-120

    Google Scholar 

  93. Zipes DP, Fischer J, King RM et al (1975) Termination of ventricular fibrillation in dogs by depolarizing a critical amount of myocardium. Am J Cardiol 36:37

    Article  PubMed  CAS  Google Scholar 

Download references

Author information

Authors and Affiliations

  1. Otto-von-Guericke-Universität Magdeburg Klinik für Kardiologie — Angiologie —, Pneumologie im Zentrum Innere Medizin, Leipziger Straße 44, 39120, Magdeburg

    S. Reek

  2. Departments of Medicine, Physiology and Biomedical Engineering, University of Alabama at Birmingham, Volker Hall, Room B 140 1670 University Boulevard, 35292-0019, Birmingham, Alabame, USA

    R. E. Ideker

Authors
  1. S. Reek
    View author publications

    You can also search for this author in PubMed Google Scholar

  2. R. E. Ideker
    View author publications

    You can also search for this author in PubMed Google Scholar

Rights and permissions

Reprints and permissions

About this article

Cite this article

Reek, S., Ideker, R.E. Mechanismen der elektrischen Defibrillation. Herzschr Elektrophys 8, 4–14 (1997). https://doi.org/10.1007/BF03042473

Download citation

  • Received:

  • Accepted:

  • Issue Date:

  • DOI: https://doi.org/10.1007/BF03042473

Schlüsselwörter

Key words

Search

Navigation