Affiliation:
1. From the Department of Biomedical Engineering (V.G.F., O.F.S., E.R.C., R.E.I.) and Department of Medicine (J.C.N., R.E.I.), University of Alabama at Birmingham, Birmingham, Ala.
Abstract
Background—
It is believed that defibrillation is due to shock-induced changes of transmembrane potential (ΔV
m
) in the bulk of ventricular myocardium (so-called virtual electrodes), but experimental proof of this hypothesis is absent. Here, intramural shock-induced ΔV
m
were measured for the first time in isolated preparations of left ventricle (LV) by an optical mapping technique.
Methods and Results—
LV preparations were excised from porcine hearts (n=9) and perfused through a coronary artery. Rectangular shocks (duration 10 ms, field strength E ≈2 to 50 V/cm) were applied across the wall during the action potential plateau by 2 large electrodes. Shock-induced ΔV
m
were measured on the transmural wall surface with a 16×16 photodiode array (resolution 1.2 mm/diode). Whereas weak shocks (E≈2 V/cm) induced negligible ΔV
m
in the wall middle, stronger shocks produced intramural ΔV
m
of 2 types. (1) Shocks with E>4 V/cm produced both positive and negative intramural ΔV
m
that changed their sign on changing shock polarity, possibly reflecting large-scale nonuniformities in the tissue structure; the ΔV
m
patterns were asymmetrical, with ΔV
−
m
>ΔV
+
m
. (2) Shocks with E>34 V/cm produced predominantly negative ΔV
m
across the whole transmural surface, independent of the shock polarity. These relatively uniform polarizations could be a result of microscopic discontinuities in tissue structure.
Conclusions—
Strong defibrillation shocks induce ΔV
m
in the intramural layers of LV. During action potential plateau, intramural ΔV
m
are typically asymmetrical (ΔV
−
m
>ΔV
+
m
) and become globally negative during very strong shocks.
Publisher
Ovid Technologies (Wolters Kluwer Health)
Subject
Physiology (medical),Cardiology and Cardiovascular Medicine
Cited by
59 articles.
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