Electrical properties of myocardium such as cardiac action potential, refractory period, cardiac impulse generation, pacemaker potentials are described
2. Introduction
• Cardiac muscle is an excitable tissue.
• Excitable tissues have the property that, on
stimulation, there is a brief reversal of resting
membrane potential, known as an action
potential.
• Action potential initiates an excitation-
contraction coupling mechanism that results
in the mechanical shortening (contraction) of
the muscle fiber.
3. Electrical Properties of
cardiac muscle fiber
• Resting membrane potential
• Action potential
• Refractory period
• All or none law
• Automaticity
• Rhythmicity
• Conductivity
4. Resting Membrane Potential
• RMP is defined as the potential
difference across the cell membrane
when the cell is “at rest”( not excited or
activated).
• RMP in neuron or nerve fiber is – 70 mV
• RMP Cardiac muscle = -80 mV
• RMP Skeletal muscle = -90 mV
5. Cardiac muscle RMP:
Ionic Basis
• Ionic basis of RMP: same as in nerve
or skeletal muscle.
• RMP is a diffusion potential.
• It is created by diffusion of K+ out of
the cell, while negatively charged
ions (proteinate, phosphate) are
held back.
7. Cardiac Action Potential
Phase 0: Depolarization
• This phase is recorded as a rapid upstroke.
• The membrane potential changes from the
resting value of –80 mV to +20 mV.
• Duration: 2 msec only.
• The rapid depolarization is caused by
opening of voltage-gated Na+ channels.
9. Cardiac Action Potential
Phase 0
• Positively charged sodium ions enter the
cardiac muscle cell following
concentration and electrical gradients
(Na+ concentration: 142 mEq/L outside
and 14 mEq/L inside and membrane
potential –80 mV inside).
• Muscle cell potential changes from -
80 to +20 mV
10. Voltage-gated Na+ channels
The voltage-gated Na+ channels have two gates:
• an outer gate that opens at the beginning of
depolarization, and
• an inner inactivating gate that closes soon
after the opening of the outer gate.
11. • The inactivating gate remains
closed till the cell membrane is
repolarized back to –60 mV.
• Prolonged closure of the
inactivating gate is responsible for
the prolonged refractory period in
the cardiac muscle.
Voltage-gated Na+ channels
12. Phases 1, 2 and 3
(Repolarization)
• The down stroke of the action potential,
(repolarization), is a slow process.
• It is completed in 200–300 msec.
• Phase 1. This is a brief initial phase of rapid
repolarization, in which the membrane potential
changes from +20 mV to –10 mV
• Phase 1 is due to opening of
voltage-gated K+ channels.
13. Phase 2
• Phase 2 is the characteristic plateau of
the cardiac action potential
• It is a prolonged phase which takes about
200 msec.
• In this phase, the membrane potential is
held relatively steady
at -20 mV
14. Phase 2
• Phase 2 results from opening of voltage-gated
Ca++ channels.
• The Ca++ influx balances the effect of K+ efflux
and hence the membrane potential remains
steady.
• The transfer of Ca++ into the cell during phase
2 has an implication in the
myocardial excitation-
Contraction coupling.
15. Phase 3
• A phase of relatively rapid repolarization.
• The membrane potential reverts back to
– 80 mV.
• This phase is caused by
(i) inactivation of Ca++ channels and
(ii) still open voltage-gated
K+ channels.
• Efflux of positively charged
potassium ions restores the
membrane potential to RMP.
16. Phase 4
• This phase is recorded as a flat baseline.
• In this phase, the membrane potential is
maintained steady at the RMP value.
• During this phase, the energy-
dependent Na+-K+ ATPase pump is
activated.
17. Phase 4
• Therefore, extra Na+ which entered the
cell during depolarization are extruded.
• K+ which left the cell during repolarization
are taken back.
• Calcium ions, which entered
the cell during plateau phase,
are also extruded by a
Na+ – Ca++ pump.
18. Refractory Period
• The cardiac muscle does not respond to
another stimulus for about 200 msec after
the beginning of an action potential. This
duration is called absolute refractory
period .
• It is related to the prolonged closure of
inactivating gate of Na+ channels soon
after the beginning of an action potential.
20. .
• Throughout contraction ( systole) and
most of diastole, cardiac muscle cannot
be stimulated, i.e. heart muscle cannot
be tetanized.
• Heart has to contract, eject blood, then
relax to receive blood for next ejection.
• Tetanized heart would be useless as a
pump ( See ppt CVS 3)
Functional significance of
prolonged period
21. All or None Law
• Cardiac action potential follows all or none
law.
• If stimuli of varying strength are applied to a
strip of cardiac muscle:
• Subthreshold stimuli fail to produce an
action potential.
• With threshold and suprathreshold stimuli,
extent of action potentials is same.
23. All or None Law
• It is due to the fact that whenever
voltage-gated Na+ channels open, they
open fully and the degree of Na+ influx is
similar irrespective of the fact that a
stimulus is of threshold strength or
suprathreshold strength
24. Automaticity and Rhythmicity
• This property not seen in skeletal muscle,
which always needs stimulation by a
motor nerve.
• Heart beats automatically and
rhythmically due to automatic and
rhythmic generation of electrical impulse
in SA node and its spread through the
conduction system.
25. Conductivity
• The conduction velocity of the action
potentials in the cardiac muscle is rather slow
(0.2–1 m/sec).
• The specialized conduction tissue of the heart
has greater conduction velocity (1–4 m/sec).
26. Origin of Cardiac impulse
• Normally SA node acts as the pacemaker
of the heart since it generates pace-
maker potential.
• Normally pacemaker potentials can be
recorded in SA node and AV node.
• SA node has the highest rate of impulse
generation ( about 75/min)
27. Origin of Cardiac impulse
• Pathologically, if SA node fails to generate an
impulse, AV node can act as pacemaker, at a
slower rate ( 60/min).
• In disease, If ventricles are electrically isolated
( His bundle damaged: Complete heart block),
lower part of His bundle or Purkinje fiber may
develop pacemaker potentials at rate of 15-
40/min ( Idioventricular rhythm).
29. Pacemaker potential
(or prepotential)
• Pacemaker potential is the name given to the
slow and gradual depolarization recorded
between two cardiac action potentials.
• The slow depolarization proceeds at a steady
rate until the “firing level” (about
• – 40 mV) is attained; and then the next action
potential is fired.
31. SA Nodal Action Potential
• SA nodal RMP – 65 mV.
• Phase 0 has much slower velocity;
• Phases 1 and 2 are absent
• Phase 3 is more gradual.
• Phase 4 shows slow depolarization proceeding
at a steady rate until the “firing level” (about –40
mV) is attained; and then the next action
potential is fired.
32. SA Nodal Action Potential
Ionic basis
• Phase 0 ( upstroke) due to opening of L (for
long lasting) Ca++ channels
• The down stroke (Phase 3) is produced by
opening of K+ channels.
• Phase 4 is due to
automatic opening of
T (for transient) Ca++
channels.
33. Regulation of Pacemaker activity
Although SA node generates cardiac
impulses spontaneously, the rate of
generation is modulated by
autonomic nerves .
35. • Sympathetic stimulation increases the
slope of pacemaker potential.
• Hence, firing level is reached sooner than
normal and the frequency of cardiac
impulses per minute increases.
• In this way, sympathetic stimulation
increases heart rate.
• Parasympathetic ( vagus) stimulation
decreases the slope of pacemaker
potential, thereby decreases the heart rate.
Regulation of Pacemaker activity
36. Spread of cardiac impulse
• The cardiac impulse, generated in the
SA node, spreads radially throughout the
myocardium of the two atria simultaneously
(like ripples in a pond), and eventually reaches
the AV node.
• Atrial depolarization is completed in
approximately 0.1 sec and is followed by atrial
contraction
38. Nodal Delay
• In the AV node, the cardiac impulse is delayed
for about 200 msec, before it spreads to the
ventricles via the bundle of His.
• Nodal delay serves a very useful function.
• It ensures that the two atria complete their
contraction and empty themselves, well
before the ventricles begin to contract.
39. Excitation of His-Purkinje system
• The Purkinje system has high conduction
velocity, 1–4 m/sec.
• Therefore, once the impulse reaches the
bundle of His, it rapidly spreads
throughout the two ventricles within
0.08–0.1 second.
40. Excitation of interventricular septum
• In the ventricles, the interventricular
septum is first to be depolarized.
• Septum’s left side is initially depolarized
and the wave of depolarization spreads
towards the right side of
the septum.
41. Excitation of ventricles
• As the impulse reaches the apex of the heart, it
returns along the subendocardial region of the two
ventricles to the AV groove.
• In the meantime, it spreads throughout the
ventricular wall from the subendocardial to the
epicardial surface.
• The His-Purkinje system has high conduction
velocity, 1–4 m/sec.
• Therefore, once the impulse reaches the bundle of
His, it rapidly spreads throughout the two ventricles
within 0.08–0.1 second.
