© 2003 by European Society of Cardiology
INVITED COMMENTARY
The relationship of defibrillation and stimulation: design implications for the optimum defibrillation waveform
Departments of Medicine, Physiology, and Biomedical Engineering, University of Alabama, Volker Hall B 140A 1670 University Blvd. Birmingham, AL 35292-0019, USA
Manuscript submitted 13 March 2003. Accepted after revision 28 March 2003.
Correspondence: Raymond E. Ideker, University of Alabama at Birmingham, 1530 3rd Ave So, VH B140, Birmingham, AL 35294-0019, U.S.A. Tel.: +1-205-975-4710; Fax: +1-205-975-4720; E-mail: rei{at}crml.uab.edu
The major point of contention in the exchange of letters to the editor by Dr Irnich and Dr Efimov and colleagues is the relationship between cardiac stimulation and defibrillation. Irnich states that the mechanisms of stimulation and defibrillation are identical while Efimov et al. state that the two phenomena are governed by fundamentally different mechanisms. We believe the relationship between stimulation and defibrillation falls between these two extremes. Specifically, we believe experimental evidence indicates that the mechanism of defibrillation encompasses the mechanism of stimulation but also includes additional factors related to the reinduction of fibrillation by the shock.
At the most basic level, stimulation and defibrillation both require the electrical pulse to alter the transmembrane potential and, thus, are similar in this respect. In both cases, the electric pulse creates regions of hyperpolarization and of depolarization, called virtual electrodes, which are important determinants of whether stimulation and defibrillation occur. Defibrillation involves extinguishing the activation fronts present during fibrillation via stimulation of excitable and partially excitable myocardium. In addition, refractory myocardium can become de-excited in an area of virtual anode and stimulated again by a closely adjacent virtual cathode. Experimental studies indicate the same events can take place during stimulation in the relative refractory period[1]
. While the initiation of a new action potential following de-excitation is a form of stimulation, Weiss' Law referred to in Irnich's letter may not apply to it, since Weiss' Law was established for stimulation of fully recovered tissue.
Even though the title of the paper by Mowrey et al. from Efimov's laboratory that led to the exchange of letters contains the word ‘defibrillation’ twice, shocks were not given during fibrillation in the study[2]. Instead, shocks were applied during various phases of the paced action potentials and measured cardiac responses were used to draw conclusions about defibrillation. As can be seen in Fig. 10 of their manuscript, some of these shocks stimulated a new action potential. Therefore, Mowrey and colleagues implicitly assumed that stimulation and defibrillation are closely related.
One difference between stimulation and defibrillation mentioned by Efimov et al. is that the voltage of the pulse required to defibrillate is almost two orders of magnitude greater than that required to stimulate. However, the primary reason for this large difference in pulse strength is that stimulation of a heart beat only requires altering the transmembrane potential in a small volume of tissue to launch an activation front that spreads to the remainder of the myocardium while defibrillation requires altering the transmembrane potential over all or most of the myocardium to halt the fibrillation activation fronts located there[3]. Experimental and simulation data suggest that the amount of change in the transmembrane potential required to defibrillate is only a few times greater than that required to stimulate a new action potential[4–6]. The reason the defibrillation threshold is so much higher than the stimulation threshold is that the change in the transmembrane potential caused by a shock rapidly decreases with distance from the defibrillation electrodes[5]. If it were possible to put defibrillation electrodes a few millimetres apart throughout the entire myocardium, the defibrillation threshold voltage might be only a few times larger than the stimulation threshold[3].
The primary difference between stimulation and defibrillation is that in addition to halting preexisting fibrillation, defibrillation also must not produce new activation fronts that reinduce fibrillation[7]. Efimov et al. believe that fibrillation is reinduced by reentry caused through the creation of virtual electrodes by the defibrillation shock. However, as discussed previously, the initiation of a reentrant activation front by the virtual electrodes is a form of stimulation by the shock.
Experimental evidence indicates that a defibrillation shock can fail for at least three additional reasons besides reinduction of reentry by the shock[8]. Weaker shocks can fail to defibrillate because they do not halt the activation fronts present during fibrillation. Stronger shocks can halt fibrillation activation fronts as well as prevent the induction of sustained reentry after the shock yet can still fail because they trigger several rapid activations after the shock that reinduce fibrillation. These activations arise focally in quick succession until they initiate reentry that first occurs several hundred msec after the shock, thereby reinducing fibrillation. Recent evidence raises the possibility that these rapid focal activations are caused by delayed afterdepolarizations triggered by the shock[9,10]. The prevention of these triggered foci requires a stronger shock than the prevention of sustained reentry and therefore, determines the defibrillation threshold. Much stronger shocks can also fail[11], possibly due to shock-induced electroporation followed by a tachyarrhythmia leading to fibrillation.
In conclusion, we believe that the mechanism of defibrillation encompasses the mechanism of stimulation since stimulation is involved in the termination of the fibrillation activation fronts present just before the shock and is involved in the reinitiation of fibrillation by reentry caused by the shock. However, the mechanism of defibrillation probably also includes the mechanism by which triggered activations are created by the shock and reinitiate fibrillation.
 |
Acknowledgements |
|---|
 Top Acknowledgements References |
|---|
Supported in part by the NHLBI Grants HL42760, HL67448, and HL63775.
|
References |
|---|
|
TopAcknowledgementsReferences |
|---|
[1] Lin SF, Roth BJ, Wikswo JP Jr. Quatrefoil reentry in myocardium: an optical imaging study of the induction mechanism. J Cardiovasc Electrophysiol 1999; 10: 574–586.[Web of Science][Medline]
[2] Mowrey KA, Cheng Y, Tchou PJ, et al. Kinetics of defibrillation shock-induced response: design implications for the optimal defibrillation waveform. Europace 2002; 4: 27–39.
[3] Ideker RE, Zhou X, Knisley SB. Correlation among fibrillation, defibrillation, and cardiac pacing. Pacing Clin Electrophysiol 1995; 18: 512–525.[CrossRef][Medline]
[4] Clark DM, Pollard AE, Ideker RE, et al. Optical transmembrane potential recordings during intracardiac defibrillation-strength shocks. J Interv Card Electrophysiol 1999; 3: 109–120.[CrossRef][Medline]
[5] Efimov IR, Cheng YN, Biermann M, et al. Transmembrane voltage changes produced by real and virtual electrodes during monophasic defibrillation shocks delivered by an implantable electrode. J Cardiovasc Electrophysiol 1997; 8: 1031–1045.[Web of Science][Medline]
[6] Evans FG, Ideker RE, Gray RA. Effect of shock-induced changes in transmembrane potential on reentrant waves and outcome during cardioversion of isolated rabbit hearts. J Cardiovasc Electrophysiol 2002; 13: 1118–1127.[CrossRef][Web of Science][Medline]
[7] Chen P-S, Shibata N, Dixon EG, et al. Activation during ventricular defibrillation in open-chest dogs: evidence of complete cessation and regeneration of ventricular fibrillation after unsuccessful shocks. J Clin Invest 1986; 77: 810–823.[Web of Science][Medline]
[8] Ideker RE, Chattipakorn N, Gray RA. Defibrillation mechanisms: the parable of the blind men and the elephant? J Cardiovasc Electrophysiol 2000; 11: 1008–1013.[Web of Science][Medline]
[9] Chattipakorn N, Fotuhi PC, Chattipakorn SC, et al. Three-dimensional mapping of earliest activation after near-threshold ventricular defibrillation shocks. J Cardiovasc Electrophysiol 2003; 14: 65–69.[CrossRef][Web of Science][Medline]
[10] Chattipakorn N and Ideker RE. Delayed afterdepolarization inhibitor: a potential pharmacological intervention to improve defibrillation efficacy. J Cardiovasc Electrophysiol 2003; 14: 72–75.[CrossRef][Web of Science][Medline]
[11] Dixon EG, Tang ASL, Wolf PD, et al. Improved defibrillation thresholds with large contoured epicardial electrodes and biphasic waveforms. Circulation 1987; 76: 1176–1184.
CiteULike 
Connotea 
Del.icio.us What's this?
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||