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A Study on Electric Field Effects on Cardiac
Muscle
Document By
SANTOSH BHARADWAJ REDDY
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Abstract—High voltage engineering(HVE) finds application
in all fields ranging from HV apparatus design, pure physics
research, food processing, medical diagnosis, gene-therapy and
targeted drug delivery etc. This study aims in an attempt to
explore the application of HVE in determining the electric field
effects on biological tissues namely cardiac muscle. The electric
field mechanism is important under “Arrhythmic” conditions.
At rest condition the resting potential of cardiac muscle is
-80mV. During excitation the action potential should overshoot
+32mV. Under “Arrhythmic” condition the magnitude of the
action potential should not overshoot +32mV. During this
condition the application of electric field mechanism combined
with gap junction mechanism to act in concrete to facilitate
transmission of excitation between the continuous cells of chain.
The Pspice model accurately depicts excitation and propagation
in cardiac muscle. Hence the cardiac muscle was simulated as
single cell and single chain 1x2 model . This study can be
further extended to single chain of 1x5 model and parallel
chains of 5x3, 5x5 model.
Index Terms—Cardiac Muscle, Excitation of Cell, Gap
junction, Simulated Action Potential, Modeling of cardiac
muscle.
INTRODUCTION
The electric field mechanism was
first proposed in 1977 by Sperelakis
and Mann[1] for the transmission of
excitation between cardiac muscle
cells. Here a study on electric field
effects on cardiac muscle is
simulated as single cell and single
chain as the 1x 2 model using
Pspice. Remodeling of conduction
pathways in the hypertrophy response to myocardial injury is
a potential mechanism leading to the development of
“Arrhythmias”. The high voltage pulsed power is used to
activate the cardiac cells during some “Arrhythmias”
conditions. In cardiac muscle, the electric field mechanism
account for propagation of excitation that do not posses gap
junctions. In the reentrant type (sudden death) of conditions
in which the gap junctions do exist and are functioning, the
electric field mechanism would act in parallel and there by
increase the safety factor for conduction. The electrical
 arrhythmic condition wave forms are shown in fig(1),fig(2).
voltage is generated in the narrow junction clefts, when the
pre junction membrane fires an Action potential, depolarizes
the post junction membrane to its threshold value. After
reaching its threshold value the inactive cell becomes active
cell then it comes under normal Rhythmic condition.
Lakshmi narayanan ramasamy et al., explained about
transverse propagation in an expanded Pspice model for
cardiac muscle with gap junction ion channels and the partial
uncoupling of heart actually improved “impulse” conduction
by converting unidirectional block to bidirectional
propagation [8].
This paper explain about the electric field in
cardiac muscle and different mechanism for transmission of
excitation, electric field model requirements and junction
cleft, patch clamp like effect. And this also explains the
action potential of cardiac muscle, resting potential, rising
phase depolarization, falling phase depolarization, refractory
period, threshold and initiation and circuit model for cell
membrane. Finally it covers the simulation of cardiac
muscle for single cell and single chain (1x2 Model) using
Pspice.
I. ELECTRIC FIELD IN CARDIC MUSCLE
Cardiac muscles are composed of an assembly of short
individual cells, separated at their ends by cell junctions. The
fluid in the junction gap is continuous with the bulk intestinal
fluid.(ISF), and the gap thickness averages about (100-
200A°).The length of the cardiac cell is assumed to be very
long(1-2mm)[1].The input resistance of one cell with in the
bundle was said to be very low(50kΩ) and the input
resistance of an isolated single cell to be very high(1-
2GΩ).The length constant is very short(150-350µm),and the
input resistance of a cell, Whether in a bundle or isolated is
about (10-40MΩ)[1].
Under “rhythmic condition” the resting potential of cardiac
muscle is -80 mV. The resting potential is mostly determined
by the ion concentrations in the fluids on both sides of the
cell membrane and the ion transport proteins in the cell
membrane. The active transport of potassium and sodium
ions into and out of the cell respectively is accomplished by a
number of sodium-potassium pumps scattered across the cell
membrane. Each pump transports two ions of potassium into
the cell for every three ions of sodium pumped out. During
excitation, the action potential should overshoot +32mV. In
“arrhythmic condition”, during excitation, the action
potential should not overshoot +32mV.The rhythmic and

Fig(1)” Rhythmic” condition waveform
Fig(2) “Arrhythmic” condition waveform
II. MECHANISM FOR TRANSMISSION OF EXCITATION IN
CARDIAC MUSCLE
A large increase in gap junctions produces only a small
increase in propagation velocity in cardiac muscle and
smooth muscles, the maximum resistance of the junction
membranes that would not allow successful transmission by
local circuit without gap junctions. Where the gap junctions
exist, they provide a conduit for passage of local circuit
current from one cell to the next (“electrical coupling”) and
for passage of molecules (“metabolic coupling”) including
injected dyes [2], [3]. That is, they undoubtedly provide one
means for transfer of excitation from cell to cell. Gap
junctions are abundant in mammalian hearts, but such
specialized contacts are rare and much smaller in hearts of
lower vertebrates. Fig (3), which depicts local circuit current
(I l c) passing through high resistance post junction, is
unlikely to allow successful transmission because most of the
current would flow out radically through the cleft and there
by pass the post cell [4].
I. CAPACITIVE COUPLING
Capacitive coupling is unlikely to be the sole mechanism
in mammalian hearts since the specific capacitance of the
post membrane would need to be considerably higher than
the known value for biological membranes (i.e., ca 0.7 – 1.0
µF/cm^2)[4].One cannot conclude about the degree of cell to
cell coupling from measurements of length constant in a
2
muscle bundle. Fig(3) in that case, the amount of current that
passes into the post cell would increase during the rising
phase of the AP in the pre cell. This is because the capacitive
reactance (X c) of the post-JM would be decreased in
accordance with
X c = 1 / 2 ∏ f c.
Fig (3)
K+ Accumulation
Capacitive K+ ions serve as a chemical messenger. During
excitation, the electrochemical driving force for net outward
K+ current increases in propagation into depolarization .
Therefore, efflux of K+ across the suddenly increase during
the rising phase of the AP, even if K+ conductance (g k)
remains constant. The potassium ions effluxing across the
surface will diffuse rapidly into and mix with the bulk ISF
[4].
II.EPHAPTIC TRANSMISSION
Impulse transmission between ventricular myocardial cells
can even occur ephaptically; i.e., by a “false synapse “with
two isolated cylindrical bundles closely appositioned for a
short distance (e.g., 800µm)[4], when one bundle after a short
distance was electrically stimulated, the impulse jumped to
the second bundle after a short delay
Interactions between neurons in vertebrate brain have been
described that are ephaptic in nature, depending on current
flow through the second neuron. It was also shown that
electrical fields caused synchronous bursting in adjacent
hippocampus neurons in which chemical transmission was
blocked [1].
III. ACTION POTENTIAL
Impulse transmission between ventricular myocardial cells
can even occur ephaptically; i.e., by a “false synapse “with
two isolated cylindrical bundles closely appositioned for a
short distance (e.g., 800µm)[3], when one bundle after a short
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distance was electrically stimulated, the impulse jumped to
the second bundle after a short delay.
Action potentials are not the same in all cell types and can
even vary in their properties at different locations in the same
cell. Fig (4) shows the schematic action potential .
excitation, the action potential should overshoot +32mV [1].
The Electrical voltage develops in narrow junction cleft,
when the membrane generates an action potential. The
electric field mechanism account for propagation of
excitation in cardiac muscle. The mechanism of cardiac
muscle is been explained in fig(5).

Fig(4) “ Schematic” Action Potential

As sodium ions enter and the membrane potential becomes
less negative, more sodium channels open, causing an even
greater influx of sodium ions. This is an example of positive
feedback. As more sodium channels open, the sodium current
dominates over the potassium. Leak current and the
membrane potential become positive inside.
Peak:
By the time the membrane potential has reached a peak
value of around +40 mV [3], voltage sensitive inactivation
gates on the sodium channels have already started to close,
reducing and finally preventing further influx of sodium ions. fig (5) flowchart for mechanism for cardiac muscle
While this occurs, the voltage sensitive activation gates on
the voltage gated potassium channels begin to open .
Falling phase repolarization: There are four basic excitable units represented
As voltage-gated potassium channels open, there is a large each cell. Two for the long surface membrane of the cell
outward movement of potassium ions driven by the (one upward facing and one downward facing). One basic
potassium concentration gradient and initially favored by the unit for each of the two junctional membranes (left end of
positive-inside electrical gradient. As potassium ions diffuse cell and right end of cell). The radial (shunt) resistance of the
out, this movement of positive charge causes a reversal of the junctional cleft (RJ c) was placed in the junctions between
membrane potential to negative-inside and depolarization of adjoining cells [9]. The basic units were connected internally
the neuron back towards the large negative-inside resting by the intracellular longitudinal resistance(R) and externally
potential. by the extra cellular resistance (Ro). This (Ro) had broken
Undershoot: down into a longitudinal component (Ro1) and a transverse
Closing of voltage gated potassium channels is both (radial) component (Ror). The structure of single cell was
voltage and time dependent. As potassium exits the cell, the
given in fig (6).
resulting membrane depolarization initiates the closing of
voltage-gated potassium channels. These channels do not
close immediately in response to a change in membrane
potential; rather, voltage- gated potassium channels have a
delayed response[3], such that potassium continues to flow
out of the cell even after the membrane has fully repolarized.
Thus the membrane potential dips below the normal resting
membrane potential of the cell for a brief moment the dip of
hyper polarization is known as the undershoot.

IV. MODELLING OF CARDIAC MUSCLE

The resting potential of cardiac muscle is –80mV. During

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V. EXCITATION OF CELL
Electrical simulations were applied internally to the first
chain, using rectangular depolarizing current pulses of 0.5-
nA amplitude and 0.5ms duration [9]. The delay time before
the current pulse was set to 1.0ms. Because the spice
program doses not have a voltage dependent resistance (to
generate the increase in K a ++ or Ca ++ conductance during
excitation), this function had to be done with a voltage
controlled current source. The sigmoid relationship between
conductance and membrane potential (V) had to be
mimicked by the black- box. The Na++ or Ca++ current
required for excitation has to be calculated for several
Voltage values and inserted into the GTABLE function [5].
The GTABLE values we originally used made the
myocardial cells and smooth muscles somewhat hyper
excitable. Therefore, in the present experiments, The
GTABLE values were altered to produce three levels of
excitability in the cells: high, intermediate, and low [9]. If
the network is larger [7], propagation by electric field
mechanism is almost as fast as in the case of strong coupling.
Hence, the transverse propagation of cardiac muscle cells in
single chain (1x2) can be extended to (1x3), (1x5) model and
parallel strands with longer chains (5x3, 5x5).The result
obtained from the single cell of cardiac muscle under
standard condition illustrated in fig(7). In this figure the AP
overshoots +32mV.

Fig(7)

Table1: Summary of values used under standard condition

Parameters Values

Input resistance(R) 20MΩ

Input capacitance(C) 100pF

Radial resistance (Ror2) 100Ω

Longitudinal resistance (Rol2) 200KΩ

Radial resistance of junction cleft (Ror2) 25MΩ

Fig (6)

Resistance of gap junction(R j I ) 10MΩ
Potassium resistance(R k) 6000MΩ
Sodium resistance(R Na) 3000MΩ
Potassium equilibrium potential (E k) -90mv
Sodium equilibrium potential (E Na) +60mv
Surface capacitance (Cs) 16pF
Junction capacitance (C j) 4pF
VI. CONCLUSION
The electric field mechanism alone can provide propagation
between excitable cells that are not connected by low-
resistance tunnels under conditions or under arrhythmic
conditions. If the network is larger, propagation by electric
field mechanism is almost as fast as in the case of strong
coupling. Hence, the transverse propagation of cardiac
muscle cells in single chain (1x2) can be extended to (1x5)
model and parallel strands with longer chains (5x3, 5x5).
From the simulation study of propagation in cardiac muscle
• The electric field is generated in the narrow clefts, when
the pre junction membrane fires an action potential,
depolarizes the membrane to its threshold.
• For strong longitudinal, coupling between the cells, we
have to increase the value of longitudinal resistance or
decrease the value of transverse resistance.
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REFERENCES
[1] N.Sperelakis and K. McConnell, ”Electric field interactions
between closely-abutting excitable cells”, IEEE-EMB vol.21,
pp.77-99, 2002.
[2] N.Sperelakis and J.E. Mann Jr., “Evaluation of electric field
changes in the cleft between excitable cells”, J. TheorBiol,
vol.64, pp.71-96, 1977.
[3] Can.J. Physiol.Pharmacol, “ Propagation of action potentials
between parallel chains of cardiac muscle cells in Pspice
simulation”, vol.81, pp.1-11, 2003
[4] Editorial:” An electric field mechanism for transmission of
excitation between myocardial cells”, Circ. Res, vol.91,
pp.985-987, 2002
[5] N.Sperelakis, “Cable properties and propagation of action
potentials”, in cell Physiology Source Book, 1st Ed: Academic
Press Publishers, 1995, ch 18, pp.245-254.
[6] N.Sperelakis and L. Ramasamy, “ Propagation in cardiac
muscle and smooth muscle based on electric field transmission
at cell junctions: An analysis by Pspice”, IEEE-EMB, vol.21,
pp.130-143, 2002.
[7] 7. J.B. Pcone, N.Sperelakis and J.E. Mann Jr, “Expanded
model of the electric field hypothesis for propagation in
cardiac muscle”, Math. & Computer Modeling, vol.15, pp.17-
35, 1991
[8] Gap junction channels inhibit transverse propagation muscle,
Nicholas Sperelakis and Lakshminarayanan Ramasamy,
Biomedical engineering online, vol.4, pp 1-11, 2004.
[9] Effect of variation in membrane excitability on propagation
velocity of simulated action potentials for cardiac muscle and
smooth muscle in the electric field model for cell to cell
transmission of excitation, IEEE transactions on Biomedical
Engg, Vol.51, no.12, December 2004.
Corresponding Author: V.kayalvizhi,Department of Electrical &
Electronics Engineering, College of Engineering, Guindy, Anna
University, Chennai25
.kayal_v71@yahoo.com, vg_sree@annauniv.edu .
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