The document describes the structure and function of cardiac muscle, highlighting its striated fibers, intercalated discs, and the unique properties of its conduction system, including pacemaker cells like the sinoatrial node. It explains how the autonomic nervous system regulates heart rate through neurotransmitters affecting ion channel conductance, as well as detailing the process of depolarization and how it generates the ECG waves. Additionally, it touches on cardiac cycle concepts and factors influencing cardiac output, stroke volume, and the effects of chronotropic and inotropic agents.

1. Cardiac Muscle and Heart Function
• Cardiac muscle fibers are striated –
sarcomere is the functional unit
• Fibers are branched; connect to one
another at intercalated discs. The
discs contain several gap junctions
• Nuclei are centrally located
• Abundant mitochondria
• SR is less abundant than in skeletal
muscle, but greater in density than
smooth muscle
• Sarcolemma has specialized ion
channels that skeletal muscle does
not – voltage-gated Ca2+ channels
• Fibers are not anchored at ends;
allows for greater sarcomere
shortening and lengthening

3. 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

4. Why are fibers of the conducting system autorhythmic?
Membrane potential of SA nodal cells
If channels
How does the
depolarization in these
cells affect cardiac muscle
cells?
Superimpose changes in
the muscle cell’s membrane
potential on this graph

5. Changes in ion concentrations in a cardiac muscle fiber following
depolarization
What causes the muscle resting
membrane potential to change
initially?
What would be happening with a
skeletal muscle at this point?

6. • 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 CAN NOT sum action potentials or contractions and can’t be tetanized

7. • 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?

9. 1
2
3
4

10. • 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

11. •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

12. •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.

15. Arhythmias can be detected with an ECG draw the others
Normal
Bradycardia
Tachycardia
Atrial fibrillation
Ventricular fibrillation
Compounds that increase or decrease rate are called chronotropic agents
Compounts that increase or decrease force of contraction are called inotropic agents

16. Cardiac Cycle http://www.physiology.wisc.edu/phys335/Cycle_11-14-99.swf

18. Atrial
volume
(ml)
100
50

19. Cardiac Output = Q = volume of blood ejected from the heart each
minute
What would I have to know to be able to determine what the cardiac
output is at rest?
What is the stroke volume?
What determines the stroke volume?
How can I alter cardiac output?

22. What causes this increase in
stroke volume?