Shock-induced epicardial and endocardial virtual electrodes leading to ventricular fibrillation via reentry, graded responses, and transmural activation.

Shock-induced epicardial and endocardial virtual electrodes leading to ventricular fibrillation via reentry, graded responses, and transmural activation.
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电击引起的心外膜和心内膜虚拟电极通过折返、分级反应和跨壁激活导致心室颤动。

DOI:
10.1046/j.1540-8167.2004.03312.x
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发表时间:
2004
期刊:
Journal of cardiovascular electrophysiology.
影响因子:
--
通讯作者:
Gray,RichardA
Gray,RichardA
中科院分区:
--
文献类型:
--
作者:
Evans,FrederickG;Gray,RichardA

文献摘要

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Introduction:The mechanism of ventricular fibrillation (VF) induction by T wave shocks has been attributed to reentry, propagated graded responses (PGR), and triggered activity. The limitation of recording transmembrane potential (Vm) from only a single surface has hampered efforts to elucidate the relative role of these phenomena and their relationship to shock‐induced virtual electrodes.Methods and Results:Vmpatterns from epicardial and endocardial surfaces of isolated sheep right ventricles were recorded with two CCD cameras for monophasic (M) and biphasic (B) shocks delivered at various coupling intervals (CI) from a unipolar mesh electrode on the epicardium. VF was induced via (1) the formation of reentry following make or break excitation; (2) propagated graded responses during apparent isoelectric window; and (3) breakthrough activation patterns coincident with endocardial‐to‐epicardial gradients inVm. M shocks depolarized both surfaces at long CIs and polarized epicardial and endocardial surfaces oppositely at short CIs. At intermediate CIs, postshockVmpatterns could lead to reentry on one surface or endocardial‐to‐epicardial gradients resulting in breakthrough. B induced VF less than M for short and intermediate CIs due to more homogeneous end‐shockVmpatterns. However, at long CIs these homogeneous patterns resulted in more VF induction because B left the tissue closer to theVmthreshold for propagation.Conclusion:Postshock activity occurred either immediately via epicardial or endocardial reentry, or after a delay caused by transmural propagation or propagated graded responses. These findings could explain the isoelectric window and focal activation patterns observed on the epicardium following VF induction shocks.(J Cardiovasc Electrophysiol, Vol. 15, pp. 79‐87, January 2004)