Effects of lidocaine on shock-induced vulnerability and defibrillation

Li Li; Vladimir Nikolski; Brian R. Wollenzier; Igor R. Efimov

Effects of lidocaine on shock-induced vulnerability and defibrillation

Li Li^*, Vladimir Nikolski, Brian R. Wollenzier, Igor R. Efimov

^*Corresponding author for this work

Biomedical Engineering

Research output: Contribution to journal › Conference article › peer-review

Abstract

Lidocaine is known to increase monophasic shock (MS) defibrillation threshold (DFT). We investigated the underlying mechanisms using optical mapping of the shock-induced arrhythmias in Langendorf-perfused rabbit hearts. MS were delivered from two mesh electrodes during pacing. Vulnerability was assessed as vulnerable window (VW) within shock strengths of 15V - 150V and vulnerable period (VP) within coupling intervals of 0 - 100% of action potential duration (%APD). Lidocaine caused significant increase in both VW (51 ± 16 V vs 100 ± 16 V, p<0.01) and VP (44 ± 21 V vs 49 ± 17 V, p<0.01). Lidocaine had no effect on virtual electrode polarization (δV_m). In contrast, the conduction velocity (CV) slowed significantly by lidocaine during both pacing (0.58 ± 0.08 m/s vs 0.44 ± 0.05 m/s, p<0.01) and shock-induced reentry (0.34 ± 0.07 m/s vs 0.19 ± 0.08 m/s, p<0.01). Slowing of the conduction caused by lidocaine resulted in increased dispersion of repolarization. Conclusions: Lidocaine increased vulnerability due to the slowing of shock-induced wavefront, which resulted in enhanced probability of survival of virtual electrode induced phase singularity. Lidocaine had no significant effect on shock-induced δV_m.

Original language	English (US)
Pages (from-to)	1451-1452
Number of pages	2
Journal	Annual International Conference of the IEEE Engineering in Medicine and Biology - Proceedings
Volume	2
State	Published - 2002
Event	Proceedings of the 2002 IEEE Engineering in Medicine and Biology 24th Annual Conference and the 2002 Fall Meeting of the Biomedical Engineering Society (BMES / EMBS) - Houston, TX, United States Duration: Oct 23 2002 → Oct 26 2002

Keywords

Electrophysiology
Lidocaine
Vulnerability

ASJC Scopus subject areas

Signal Processing
Biomedical Engineering
Computer Vision and Pattern Recognition
Health Informatics

Cite this

@article{b9f70dae61b1430b9024a775b84a9ba3,

title = "Effects of lidocaine on shock-induced vulnerability and defibrillation",

abstract = "Lidocaine is known to increase monophasic shock (MS) defibrillation threshold (DFT). We investigated the underlying mechanisms using optical mapping of the shock-induced arrhythmias in Langendorf-perfused rabbit hearts. MS were delivered from two mesh electrodes during pacing. Vulnerability was assessed as vulnerable window (VW) within shock strengths of 15V - 150V and vulnerable period (VP) within coupling intervals of 0 - 100% of action potential duration (%APD). Lidocaine caused significant increase in both VW (51 ± 16 V vs 100 ± 16 V, p<0.01) and VP (44 ± 21 V vs 49 ± 17 V, p<0.01). Lidocaine had no effect on virtual electrode polarization (δVm). In contrast, the conduction velocity (CV) slowed significantly by lidocaine during both pacing (0.58 ± 0.08 m/s vs 0.44 ± 0.05 m/s, p<0.01) and shock-induced reentry (0.34 ± 0.07 m/s vs 0.19 ± 0.08 m/s, p<0.01). Slowing of the conduction caused by lidocaine resulted in increased dispersion of repolarization. Conclusions: Lidocaine increased vulnerability due to the slowing of shock-induced wavefront, which resulted in enhanced probability of survival of virtual electrode induced phase singularity. Lidocaine had no significant effect on shock-induced δVm.",

keywords = "Electrophysiology, Lidocaine, Vulnerability",

author = "Li Li and Vladimir Nikolski and Wollenzier, {Brian R.} and Efimov, {Igor R.}",

year = "2002",

language = "English (US)",

volume = "2",

pages = "1451--1452",

journal = "Annual International Conference of the IEEE Engineering in Medicine and Biology - Proceedings",

issn = "1557-170X",

publisher = "Institute of Electrical and Electronics Engineers Inc.",

note = "Proceedings of the 2002 IEEE Engineering in Medicine and Biology 24th Annual Conference and the 2002 Fall Meeting of the Biomedical Engineering Society (BMES / EMBS) ; Conference date: 23-10-2002 Through 26-10-2002",

}

TY - JOUR

T1 - Effects of lidocaine on shock-induced vulnerability and defibrillation

AU - Li, Li

AU - Nikolski, Vladimir

AU - Wollenzier, Brian R.

AU - Efimov, Igor R.

PY - 2002

Y1 - 2002

N2 - Lidocaine is known to increase monophasic shock (MS) defibrillation threshold (DFT). We investigated the underlying mechanisms using optical mapping of the shock-induced arrhythmias in Langendorf-perfused rabbit hearts. MS were delivered from two mesh electrodes during pacing. Vulnerability was assessed as vulnerable window (VW) within shock strengths of 15V - 150V and vulnerable period (VP) within coupling intervals of 0 - 100% of action potential duration (%APD). Lidocaine caused significant increase in both VW (51 ± 16 V vs 100 ± 16 V, p<0.01) and VP (44 ± 21 V vs 49 ± 17 V, p<0.01). Lidocaine had no effect on virtual electrode polarization (δVm). In contrast, the conduction velocity (CV) slowed significantly by lidocaine during both pacing (0.58 ± 0.08 m/s vs 0.44 ± 0.05 m/s, p<0.01) and shock-induced reentry (0.34 ± 0.07 m/s vs 0.19 ± 0.08 m/s, p<0.01). Slowing of the conduction caused by lidocaine resulted in increased dispersion of repolarization. Conclusions: Lidocaine increased vulnerability due to the slowing of shock-induced wavefront, which resulted in enhanced probability of survival of virtual electrode induced phase singularity. Lidocaine had no significant effect on shock-induced δVm.

AB - Lidocaine is known to increase monophasic shock (MS) defibrillation threshold (DFT). We investigated the underlying mechanisms using optical mapping of the shock-induced arrhythmias in Langendorf-perfused rabbit hearts. MS were delivered from two mesh electrodes during pacing. Vulnerability was assessed as vulnerable window (VW) within shock strengths of 15V - 150V and vulnerable period (VP) within coupling intervals of 0 - 100% of action potential duration (%APD). Lidocaine caused significant increase in both VW (51 ± 16 V vs 100 ± 16 V, p<0.01) and VP (44 ± 21 V vs 49 ± 17 V, p<0.01). Lidocaine had no effect on virtual electrode polarization (δVm). In contrast, the conduction velocity (CV) slowed significantly by lidocaine during both pacing (0.58 ± 0.08 m/s vs 0.44 ± 0.05 m/s, p<0.01) and shock-induced reentry (0.34 ± 0.07 m/s vs 0.19 ± 0.08 m/s, p<0.01). Slowing of the conduction caused by lidocaine resulted in increased dispersion of repolarization. Conclusions: Lidocaine increased vulnerability due to the slowing of shock-induced wavefront, which resulted in enhanced probability of survival of virtual electrode induced phase singularity. Lidocaine had no significant effect on shock-induced δVm.

KW - Electrophysiology

KW - Lidocaine

KW - Vulnerability

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M3 - Conference article

AN - SCOPUS:0036915931

SN - 1557-170X

VL - 2

SP - 1451

EP - 1452

JO - Annual International Conference of the IEEE Engineering in Medicine and Biology - Proceedings

JF - Annual International Conference of the IEEE Engineering in Medicine and Biology - Proceedings

T2 - Proceedings of the 2002 IEEE Engineering in Medicine and Biology 24th Annual Conference and the 2002 Fall Meeting of the Biomedical Engineering Society (BMES / EMBS)

Y2 - 23 October 2002 through 26 October 2002

ER -

Effects of lidocaine on shock-induced vulnerability and defibrillation

Abstract

Keywords

ASJC Scopus subject areas

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