Electrical Activity of the

Heart

Outline
Overview of the cardiovascular
system.
Review of nerve action potentials.
Action potential propagation through
the heart.
ECG

Learning Objectives
Describe the course of a cardiac impulse
through the heart.
Understand how the Na+, K+, and Ca2+
channels function in sinoatrial and
ventricular action potentials.
Know the times a cardiac impulse appears
in each part of the heat.
Know the relationship of atrial and
ventricular contraction to the ECG waves.

Cardiovasc
ular
System
Keep in mind the full
system when
studying details.
What does the heart
need to do?
What signal initiates
contraction?
Must be an
automatic signal.
Rhythmical
excitation of the
heart.
The normal
electrocardiogram

Flow of
Electrical
Signals in the
Heart
First, atria contract to fill
ventricles.
Then, ventricles contract to
send blood to the lungs and
peripheral circulation.
S-A node generates the
signal.
Signal travels through
internodal pathways and
atrial muscle (atria
contract).
A-V node and bundle delay
the signal and send it to the
ventricles.
Purkinje fibres rapidly carry
the signal throughout the
ventricles, where it then
spreads, causing
contraction.

Propagation of Electrical Signals in

Heart Muscle
Heart muscle is syncytial

ardiac Muscle

Branching cells
One or two nuclei per cell
Striated
Involuntary
Medium speed contractions

Cardiac Muscle
Found only in heart where it forms a thick layer
called the myocardium
Striated fibers that branch
Each cell usually has one centrally-located
nucleus
Fibers joined by intercalated disks
IDs are composites of desmosomes and gap junctions
Allow excitation in one fiber to spread quickly to
adjoining fibers

Under control of the ANS (involuntary) and

endocrine system (hormones)
Some cells are autorhythmic
Fibers spontaneously contract (aka Pacemaker cells)

Cardiac Muscle Tissue

Properties of Cardiac Muscle Fibers

Excitation-Contraction Coupling and Relaxation of

Cardiac Muscle

Excitation-Contraction Coupling

How are cardiac contractions started? Cardiac conduction system

Specialized muscle cells
pace the rest of the heart;
cells contain less actin and
myosin, are thin and pale
microscopically
Sinoatrial (SA) node; pace of
about 65 bpm
Internodal pathways connect
SA node to atrioventricular
(AV) node
AV node could act as a
secondary pacemaker;
autorhythmic at about 55
bpm
Bundle of His
Left and right bundle
branches
ALL
CONDUCTION FIBERS
Purkinje fibers;
CONNECTED
TO also
MUSCLE FIBERS
THROUGH
GAPatJUNCTIONS
autorhythmic
about 45 IN THE
INTERCALATED
DISCS
bpm

Action Potentials (APs)

APs are the electrical signals that we have
been discussing.
Review nerve AP on next slide.
Should know the following:
- Membrane potential
- Nernst equation
- Na+, K+, and Ca2+ channels
- Na+/K+ ATPase
New material will be APs in the SA node and
ventricles.

Nerve Action Potential

Note: membrane potentials are measured inside-outside. This will be importa

Remember when we discuss ECGs.

Sinoatrial Node
Pacemaker of the
heart.
Flattened
ellipsoid strip of
cells on the right
atrium.
No contractile
filaments.
Electrically
connected to
atrium.

Sinoatrial Node
Action Potential
Phase 4: slow
depolarization due to Na+
and Ca2+ leak until
threshold. Note fast Na+
channels are inactive at
-60 to -40 mV.
Phase 0: at threshold,
Ca2+ channels open.
Phase 3: As in nerves, K+
channels open during
repolarization.
Finally, note the slow rise
and fall of the SA AP
compared to that of the
nerve AP, and the
rhythmic firing.

AV Node and Bundle

Delays AP from reaching the ventricles, allowing the atria to empty blood into
ventricles before the ventricles contract.

Purkinje Fibres
Receives the AP from
the AV bundle and
rapidly transmits the
impulse through the
ventricles.

Impulses in
Ventricles
At the termination of
the Purkinje fibres, the
impulse rapidly travels
through the ventricle
muscle fibres via gap
junctions, from the
inside (endocardium)
to the outside
(epicardium).
The rapid propagation
of the cardiac impulse
through the Purkinje
fibres and ventricles is
important for an
effective contraction.

Ventricular AP
Phase 4: resting
membrane potential
near the K+ equilibrium
potential.
Phase 0: depolarizing
impulse activates fast
Na+ channels and
inactivates K+ channels.
Phase 1: Transient
opening of K+ channels
and Na+ channels begin
to close.
Phase 2: Ca2+ channels
are open, key difference
between nerve AP.
Phase 3: repolarization,
Ca2+ inactivate and K+
channels open.
Refractory period: Na+
channels are inactive
until membrane is
repolarized.

 The refractory period is short in skeletal muscle, but very long in

cardiac muscle.
This means that skeletal muscle can undergo summation and tetanus,
via repeated stimulation
Cardiac muscle CANNOT sum action potentials or contractions and
cant be tetanized

Cardiac Muscle

Properties of Cardiac Muscle fibers

Electrical Events
Autorhythmicity of Cells important to
understand, some cardiac drugs work at this level.

Sequence of Excitation

Modifying the Basic Rhythm: Extrinsic

Inervation of the Heart

 Autonomic nervous system modulates the frequency of

depolarization of pacemaker
Sympathetic stimulation (neurotransmitter =
binds to 1 receptors on the SA nodal membranes

);

Parasympathetic stimulation (neurotransmitter =

); binds
to muscarinic receptors on nodal membranes; increases
conductivity of K+ and decreases conductivity of Ca2+
How do these neurotransmitters get these results?

Electrocardiography (EKG)
Examines how Depolarization
occurs in the Heart

ECG examines how depolarization events occur in the heart

If a wavefront of
depolarization travels towards
the electrode attached to the
+ input terminal of the ECG
amplifier and away from the
electrode attached to the terminal, a positive deflection
will result.
If the waveform travels away
from the + terminal lead
towards the - terminal, a
negative going deflection will
be seen.
If the waveform is travelling in
a direction perpendicular to
the line joining the sites where
the two leads are placed, no
deflection or a biphasic
deflection will be produced.

The electrical activity of the heart

originates in the sino-atrial node. The
impulse then rapidly spreads through
the right atrium to the atrioventricular
node. (It also spreads through the
atrial muscle directly from the right
atrium to the left atrium.) This
generates the P-wave
The first area of the ventricular muscle to be activated is the interventricular septum, which activates from left to right. This
generates the Q-wave
Next the bulk of the muscle of both ventricles gets activated, with the endocardial surface being activated before the epicardial
surface. This generates the R-wave
A few small areas of the ventricles are activated at a rather late stage. This generates the S-wave
Finally, the ventricular muscle repolarizes. This generates the T-wave

 Since the direction of atrial depolarization is almost exactly parallel to

the axis of lead II (which is from RA to LL), a positive deflection (P wave)
would result in that lead.
Since the ventricular muscle is much thicker in the left than in the right
ventricle, the summated depolarization of the two ventricles is
downwards and toward the left leg: this produces again a positive
deflection (R-wave) in lead II, since the depolarization vector is in the
same direction as the lead II axis.
Septal depolarization moves from left to right, the depolarization vector
is directed towards the - electrode of lead II (RA), and therefore a
negative deflection (Q-wave) is produced.

Electrocardiography