How Epicardial Electrodes Influence the Transmembrane Potential
During a Strong Shock
SALIL G. PATEL
1
and BRADLEY J. ROTH
2
1
G.W.C. School of Engineering, Johns Hopkins University, Baltimore, MD and
2
Department of Physics, Oakland University,
Rochester, MI
(Received 25 April 2001; accepted 2 August 2001)
Abstract—This paper analyzes a possible artifact that may
corrupt experiments studying defibrillation of the heart. Our
hypothesis is that surface recording electrodes can influence the
transmembrane potential during a shock. In the vicinity of an
electrode, current leaves the intracellular space to take advan-
tage of the low resistance of the extracellular path, thereby
depolarizing the tissue. We calculate the transmembrane poten-
tial induced around a circular electrode when exposed to a
uniform electric field. The bidomain model represents the elec-
trical behavior of the cardiac tissue, and we account for elec-
trode polarization impedance. Our results show that adjacent
regions of depolarization and hyperpolarization exist around the
electrode, and that the induced depolarization is greater than
100 mV for a 0.5 mm radius silver–silver chloride electrode in
a 500 V/m electric field. We conclude that surface electrodes
may produce artifacts during experiments designed to study
defibrillation-strength electrical shocks. © 2001 Biomedical
Engineering Society. DOI: 10.1114/1.1415520
Keywords—Bidomain, Electrode, Heart, Cardiac, Shock.
INTRODUCTION
Many defibrillation experiments consist of shocking
the heart and then recording the electrical response using
epicardial surface electrodes.
1– 6,8,13,15,16,22–25,28,29
The im-
plicit assumption underlying these experiments is that the
recording electrodes do not influence the response of the
cardiac tissue. Our hypothesis is that in some situations
surface electrodes can influence the transmembrane po-
tential during a defibrillation shock. If this is the case,
then the act of recording the potential perturbs the elec-
trical response of the heart. The response might have
been different if the electrodes had not been present.
The mechanism responsible for this artifact is that the
epicardial electrode shorts out the extracellular space
Fig. 1a. During a shock, current far from the elec-
trode is distributed between the intracellular and extra-
cellular spaces according to their respective conductivi-
ties. However, in the vicinity of an epicardial electrode,
current leaves the intracellular space to take advantage of
the low resistance of the extracellular path, thereby de-
polarizing the tissue. The tissue hyperpolarizes where the
current reenters the tissue and redistributes back into the
intracellular space. No net current passes into the elec-
trode. Instead, current enters one side and exits the other,
using the electrode as a low resistance shunt.
One factor that influences our hypothesis is electrode
polarization impedance.
19
If this impedance is large, then
the electrode does not constitute a low resistance path,
current does not redistribute from the intracellular to the
extracellular space, and the electrode does not induce a
transmembrane potential. The polarization impedance de-
pends on the frequency and the electrode material. Dif-
ferent research groups use different materials, including
silver–silver chloride,
16,25
stainless steel,
1,13,15
and
copper.
27
Also, the electrode size relative to the length
constant of the tissue is important. Typical electrode di-
ameters range from 250 Ref. 16 to 700 m,
27
which
are similar to the length constant. We model electrode
polarization impedance by a parallel conductance per
unit area and capacitance per unit area at the electrode–
tissue interface Fig. 1b. The value for the polarization
impedance is taken from the literature.
7
We consider both
polarizable and nonpolarizable electrodes.
METHODS
We use a three-dimensional model of cardiac tissue
for calculating the transmembrane potential V
m
and the
extracellular potential V
e
Fig. 2. The bidomain model
represents the electrical properties of the tissue
14
• g
˜
e
V
e
=-
G
m
V
m
+C
m
V
m
t
, 1
• g
˜
i
+g
˜
e
V
e
=- • g
˜
i
V
m
, 2
where g
˜
i
and g
˜
e
are the intracellular and extracellular
conductivity tensors g
ix
=g
ex
=0.1863, g
iy
=g
iz
Address correspondence to Brad Roth, Department of Physics, Oak-
land University, 190 SEB, Rochester, MI 48309. Electronic mail:
roth@oakland.edu
Annals of Biomedical Engineering, Vol. 29, pp. 1028–1031, 2001 0090-6964/2001/2911/1028/4/$15.00
Printed in the USA. All rights reserved. Copyright © 2001 Biomedical Engineering Society
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