Electrical Activity of the Heart

1. Electrical Activity of the Heart
By
SATHISHKUMAR G
(sathishsak111@gmail.com)

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

3. 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.

4. Cardiovascular
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

5. 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.

6. Propagation of Electrical Signals in
Heart Muscle
• Heart muscle is syncytial

7. Cardiac Muscle
• Branching cells
• One or two nuclei per cell
• Striated
• Involuntary
• Medium speed contractions

8. 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)

9. Cardiac Muscle Tissue

10. Properties of Cardiac Muscle Fibers

11. Excitation-Contraction Coupling and Relaxation of Cardiac
Muscle

12. Excitation-Contraction Coupling

13. 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
• Purkinje fibers; also autorhythmic at
about 45 bpm
ALL CONDUCTION FIBERS CONNECTED TO
MUSCLE FIBERS THROUGH GAP JUNCTIONS IN
THE INTERCALATED DISCS

14. 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.

15. Nerve Action Potential
Note: membrane potentials are measured inside-outside. This will be important to
Remember when we discuss ECGs.

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

18. 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.

19. AV Node and Bundle
Delays AP from reaching the ventricles, allowing the atria to empty blood into
ventricles before the ventricles contract.

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

21. 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.

22. 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.

23. • 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 can’t be tetanized

24. Cardiac Muscle

25. Properties of Cardiac Muscle fibers

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

33. 1
2
3
4

34. Sequence of Excitation

35. Modifying the Basic Rhythm: Extrinsic Inervation of the
Heart

36. • Autonomic nervous system modulates the frequency of depolarization of
pacemaker
• Sympathetic stimulation (neurotransmitter = ); binds to b1 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?

38. Electrocardiography (EKG)
Examines how Depolarization occurs
in the Heart

42. • 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.
ECG examines how depolarization events occur in the heart

44. •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

45. •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.

48. Electrocardiography